Academic literature on the topic 'Immune system genes'
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Journal articles on the topic "Immune system genes"
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McTaggart, Seanna J., Darren J. Obbard, Claire Conlon, and Tom J. Little. "Immune genes undergo more adaptive evolution than non-immune system genes in Daphnia pulex." BMC Evolutionary Biology 12, no. 1 (2012): 63. http://dx.doi.org/10.1186/1471-2148-12-63.
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Borodin, А. М., Ya I. Alekseev, K. E. Gerasimov, N. V. Konovalova, E. V. Тerentjeva, D. N. Efimov, Zh V. Emanuilova, L. I. Tuchemskiy, A. A. Komarov, and V. I. Fisinin. "Chickens productivity selection affects immune system genes." Vavilov Journal of Genetics and Breeding 24, no. 7 (December 6, 2020): 755–60. http://dx.doi.org/10.18699/vj20.670.
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The quantitative trait loci associated with the immune properties of chickens are of interest from the point of view of obtaining animals resistant to infectious agents using marker-assisted selection. In the process of selecting markers for genomic selection in broiler-type chickens, a non-standard genotype frequency of the RACK1 gene allele (SNP Gga_rs15788101) in the B5 line of broiler-type chicken cross Smena 8 was identified and it was suggested that this gene was involved in selection. Therefore, it was decided to investigate the available polymorphisms in the three genes responsible for the IgY titer (DMA, RACK1 and CD1B). Molecular typing of single nucleotide polymorphisms of three loci revealed an approach to fixation of the unfavorable allele of the DMA gene (SNP Gga_rs15788237), an approach to fixation of the unfavorable allele of the RACK1 gene and the prevalence of the favorable CD1B gene allele (SNP Gga_rs16057130). Analysis of the haplotypes revealed a strong linkage disequilibrium of these genes. This suggests that these genes experience selection pressure. Analysis of the protein-coding sequences of the CD1B and DMA genes of various breeds of chickens revealed a negative selection of these genes. In order to understand whether the fixation of the studied alleles is the result of artificial selection of the B5 line of the cross Smena 8, an analysis of similar loci in layer chickens Hisex White was carried out. The frequencies of the alleles at the loci of the CD1B gene (Gga_rs16057130) and the RACK1 gene (Gga_rs15788101) in the Hisex White chicken genome differ from the frequencies of the alleles obtained for chickens of the B5 line of the cross Smena 8. It can be assumed that the fixation of the allele in the DMA gene (SNP Gga_rs15723) is associated with artificial or natural selection, consistent in broilers and layers. Changes in the loci Gga_rs16057130 and Gga_rs15788101 in the B5 line of the Smena 8 chickens are most likely associated with artificial selection of broiler productivity traits, which can subsequently lead to fixation of alleles at these loci. Artificial breeding of chickens leads to degradation of the variability of genes encoding elements of the immune system, which can cause a decrease in resistance to various diseases. The study of the negative impact of selection of economic traits on immunity should provide means to mitigate negative consequences and help find ways to obtain disease-resistant animals.
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TIFFIN, P., and D. MOELLER. "Molecular evolution of plant immune system genes." Trends in Genetics 22, no. 12 (December 2006): 662–70. http://dx.doi.org/10.1016/j.tig.2006.09.011.
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Sykes, Gina P., Joseph Kamtchum-Tatuene, Sarina Falcione, Sarah Zehnder, Danielle Munsterman, Boryana Stamova, Bradley P. Ander, Frank R. Sharp, and Glen Jickling. "Aging Immune System in Acute Ischemic Stroke." Stroke 52, no. 4 (April 2021): 1355–61. http://dx.doi.org/10.1161/strokeaha.120.032040.
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Background and Purpose: With advancing age, alterations occur to the immune system, including an increase in inflammation (inflammaging) and a reduced ability to respond to new immune challenges. The role of an aging immune system in patients with ischemic stroke remains unclear, although age is an important determinant of stroke risk and outcome. This study assessed the aging immune system in patients with acute ischemic stroke by differences in leukocyte gene expression in relationship to age. Methods: Peripheral blood RNA from 2 cohorts with acute ischemic stroke was measured by whole-genome microarray, and genes associated with advancing age were identified (false discovery rate-corrected P <0.05, partial correlation coefficient <|0.3|). Genes were characterized by pathway analysis and compared with age-associated genes from nonstroke studies (n=3974). Results: There were 166 genes associated with age in cohort 1 (derivation cohort, n=94). Sixty-nine of these age-associated genes were verified in cohort 2 (validation cohort, n=79). Identified genes included a decrease in CR2 , CD27 , CCR7 , and NT5E . Genes were associated with altered B-cell receptor signaling, lymphocyte proliferation, and leukocyte homeostasis. Forty-three of the 69 age-associated genes in stroke were also associated with age in nonstroke studies. Conclusions: A relationship between leukocyte gene expression and age in patients with ischemic stroke was identified. The changes include alterations to the adaptive humoral immune system, which may influence age-related stroke risk and outcome.
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Clark, Andrew G., and Lei Wang. "Molecular Population Genetics of Drosophila Immune System Genes." Genetics 147, no. 2 (October 1, 1997): 713–24. http://dx.doi.org/10.1093/genetics/147.2.713.
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A striking aspect of many vertebrate immune system genes is the exceptionally high level of polymorphism they harbor. A convincing case can be made that this polymorphism is driven by the diversity of pathogens that face selective pressures to evade attack by the host immune system. Different organisms accomplish a defense against diverse pathogens through mechanisms that differ widely in their requirements for specific recognition. It has recently been shown that innate defense mechanisms, which use proteins with broad-spectrum bactericidal properties, are common to both primitive and advanced organisms. In this study we characterize DNA sequence variation in six pathogen defense genes of Drosophila melanogaster and D. mauritiana, including Andropin; cecropin genes CecA1, CecA2, CecB, and CecC; and Diptericin. The necessity for protection against diverse pathogens, which themselves may evolve resistance to insect defenses, motivates a population-level analysis. Estimates of variation levels show that the genes are not exceptionally polymorphic, but Andropin and Diptericin have patterns of variation that differ significantly from neutrality. Patterns of interpopulation and interspecific differentiation also reveal differences among the genes in evolutionary forces.
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Staudt, Louis M., and Richard A. Flavell. "Genomics, Genetics, and Genes of the Immune System." Immunity 15, no. 3 (September 2001): 335–36. http://dx.doi.org/10.1016/s1074-7613(01)00204-7.
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Rosen, Haim, Oded Behar, and Haim Ovadia. "Expression of neuropeptide genes in the immune system." Journal of Neuroimmunology 35 (January 1991): 74. http://dx.doi.org/10.1016/0165-5728(91)90973-b.
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Schlenke, Todd A., and David J. Begun. "Natural Selection Drives Drosophila Immune System Evolution." Genetics 164, no. 4 (August 1, 2003): 1471–80. http://dx.doi.org/10.1093/genetics/164.4.1471.
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Abstract Evidence from disparate sources suggests that natural selection may often play a role in the evolution of host immune system proteins. However, there have been few attempts to make general population genetic inferences on the basis of analysis of several immune-system-related genes from a single species. Here we present DNA polymorphism and divergence data from 34 genes thought to function in the innate immune system of Drosophila simulans and compare these data to those from 28 nonimmunity genes sequenced from the same lines. Several statistics, including average KA/KS ratio, average silent heterozygosity, and average haplotype diversity, significantly differ between the immunity and nonimmunity genes, suggesting an important role for directional selection in immune system protein evolution. In contrast to data from mammalian immunoglobulins and other proteins, we find no strong evidence for the selective maintenance of protein diversity in Drosophila immune system proteins. This may be a consequence of Drosophila’s generalized innate immune response.
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Arystanbay, Ayaulym Adylgazykyzy, Assel Zhumina, and Valeriya Klunnaya. "Vitamin D and its influence on human immune system." Bulletin of the Karaganda University. “Biology, medicine, geography Series” 106, no. 2 (June 30, 2022): 34–45. http://dx.doi.org/10.31489/2022bmg2/34-45.
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This review presents modern domestic and foreign studies of vitamin D levels effect on the human immune system. Numerous data are presented on the participation of vitamin D in the regulation of immune responses. In recent years, more and more attention has been paid to the problem of vitamin D deficiency in the body of patients with autoimmune diseases. The significance of vitamin D in immune regulation is confirmed by the results of many experimental studies, clinical and epidemiological observations that demonstrate the relationship between low levels of the vitamin D and increased susceptibility to various infections, as well as the activity of the infectious process of viral, bacterial, and fungal etiology. Vitamin D acts both directly and indirectly on immune cells such as B and T lymphocytes, dendritic cells and macrophages. The review focuses on the molecular mechanisms of activation of the immune response under the influence of vitamin D. Vitamin D exerts its effect through binding to the vitamin D receptor (VDR), which, in turn, together with other proteins, activates the transcription of protein genes involved in the body’s immune response. In this regard, it is necessary to draw the attention of researchers to the problem of the daily intake of vitamin D, especially in a pandemic situation.
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Strelnikov, Nikolay A., Evgeniy V. Mikhaylov, Mikhail Yu Syromyatnikov, Nadezhda V. Pasko, Vera V. Strebkova, and Viktoriya V. Zhukova. "GENES THAT REGULATE THE IMMUNE SYSTEM IN FISH (REVIEW)." BULLETIN OF VETERINARY PHARMACOLOGY 1, no. 18 (2022): 127–39. http://dx.doi.org/10.17238/issn2541-8203.2022.1.127.
Full textDissertations / Theses on the topic "Immune system genes"
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Wiltshire, Carolyn. "Molecular screens for the isolation of genes involved in Candida albicans morphogenesis." Thesis, University of Aberdeen, 1999. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU536131.
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Using two related dominant negative screens, galactose-negative cDNAs were isolated that contained C. albicans TUB2 (beta-tubulin), NHP6 (non-histone protein 6), CIT2 (citrate synthase) and MRPS9 (mitochondrial ribosomal protein S9) sequences. CaTUB2 encodes beta-tubulin, a component of the microtubule system of the cytoskeleton. Overexpression of this sequence in S. cerevisiae resulted in lethality associated with cell shape changes characteristics of an arrest in the G2/M phase of the cell division cycle. However, overexpression of an ADH1-CaTUB2 fusion in C. albicans did not affect cell shape. CaNHP6 encodes a protein that shows a high level of sequence identity to ScNhp6A and ScNhp6B, and is closely related to High Mobility Group proteins from other eukaryotes. CaNHP6 overexpression in S. cerevisiae cells caused cell cycle arrest. Expression of an ADH1-CaNHP6 fusion in C. albicans did not affect growth rate, but affected both of cell and colony morphogenesis. These effects were not dependent upon the PKC pathway. CaMRPS9 encodes a protein of the small mitochondrial ribosome subunit, and overexpression of this protein caused the slow development of galactose lethality in S. cerevisiae. The development of lethality correlated with the emergence of petite mutants, indicating that the overexpression of CaMRPS9 interferes with S. cerevisiae mitochondrial function, thereby preventing growth on galactose. Similarly, CaCIT2 expression was presumed to block growth of S. cerevisiae on galactose by interfering with respiratory metabolism. Separate approaches were taken to isolate CaGCN4. This gene was of interest because (a) hypha-specific promoters contain GCRE-like sequences [Gcn4 Response Element], (b) amino acid starvation promotes yeast-to-hypha morphogenesis, and (c) GCN-like responses are thought to occur in C. albicans. The 5'-truncated C. albicans GCN4 cDNA was isolated by functional complementation of a S. cerevisiae Delta gcn4 mutation. The 5'-region of the CaGCN4 ORF, including 624 bp of 5'-untranslated region, was isolated by PCR. The sequences of the overlapping 5' and 3'fragments revealed a major ORF capable of encoding a 323 aa protein with significant homology in its C-terminal bZIP domain to ScGcn4 and other fungal Gcn4-like proteins. The existence of this ORF in the C. albicans genome was confirmed by PCR. The CaGCN4 cDNA contained two upstream ORFs and was encoded by a single exon. The contribution of C. albicans Gcn4 to yeast-to-hypa morphogenesis remains to be verified.
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Woolfson, Adrian. "Natural and artificial forms of human CD1 genes." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282946.
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Syed, Nelofer. "Development of systems to conditionally silence genes in the immune system of the mouse." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406646.
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Alvarez, Contreras Carlos Alberto. "HOST-MICROBIOME INTERACTIONS AND REGULATION OF THE IMMUNE SYSTEM." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1600446008947681.
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Pereira, Lucas Campana. "Busca de genes associados à resposta ao teste de Montenegro para antígenos de Leishmania." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42135/tde-27022013-155152/.
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O presente trabalho visa, através de métodos genético-epidemiológicos, identificarem genes associados à resposta ao antígeno da Leishmania. Utilizando amostras através do teste de Montenegro dos municípios de Monte Negro (RO) e Assis Brasil (AC). Na primeira abordagem foram feitos testes com TaqManÒ e a segunda com GWAS, e análises de associação foram feitas utilizando-se o pacote SPSS e o Plink. Não foram encontradas associações com cinco SNPs (MYD88, IL12, IL10, IFNGR1 e NRAMP1). A análise de dados de varredura genômica com filtros, indicou uma região no cromossomo 10 com 3 SNPs próximos que fazem parte de uma região regulatória que com o posterior auxilio do real time não se confirmaram, apesar do ensaio RS11251056 apresentar valores limítrofes, se tornando uma possível indicação para trabalhos futuros e por fim a último teste foi a meta-análise, através do método de Woolf, apresentou resultados indicativos de associação para ensaios encontrados no cromossomo 2 com ZNF638 relacionados a diferenciação celular e também no cromossomo 10 que contem lincRNAs e o gene NGR3, com dois ensaios apresentando valores significativos de p, onde podemos inferir que estas duas regiões podem participar ativamente na diferenciação da resposta ao antígeno da Leishmania.The present study aims, through genetic-epidemiological methods, to identify genes associated with response to Leishmania antigen. Using samples Montenegro skin test through the municipalities of Monte Negro (RO) and Assis Brazil (AC). In the first approach were tested with TaqManÒ and the second GWAS, and association analyzes were performed using SPSS and Plink. No associations were found with five SNPs (MyD88, IL12, IL10, IFNGR1, and NRAMP1). The analysis of genome scan data with filters, indicated a region on chromosome 10 with three nearby SNPs that are part of a regulatory region that later with the help of real time is not confirmed, although the test rs11251056 have borderline values, becoming an possible direction for future work and finally the last test was the meta-analysis by the method of Woolf, presented results indicating the association found in tests for chromosome 2 with ZNF638 related to cell differentiation and also on chromosome 10 that contains lincRNAs and gene NGR3, two runs with a significant p value, where we can infer that these two regions can actively participate in the differentiation of the response to Leishmania antigen.
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Watherston, Oliver Gavin. "The effect of small DNA tumour virus oncoprotiens on the expression of genes involved in the immune system." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535132.
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Lo, Amanda Susana. "Role of Genes in the Jak-Stat Pathway in the Innate Immune System and Immunosenescence in Drosophila melanogaster." Thesis, University of Maryland, Baltimore County, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10275514.
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For many organisms, the immune system tends to deteriorate with age, leading to higher susceptibility to foreign pathogens. While several biological pathways are associated with immunity, the components of the Janus-kinase-Signal Transducers and Activators of Transcription (JAK-STAT) pathway on immunity at different age groups is unclear. This study explored the knock down effects of the Drosophila JAK-STAT pathway components and a candidate gene, robo3, in blood cells. Assessments of immune function were conducted through bacterial clearance assays and phagocytosis assay at one-week and five-weeks of age. This study suggests that some JAK-STAT pathway components important in other cell types seem to have less of a role in blood cells and immunity.
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Baú, Carlos Eduardo Giuliani. "IDENTIFICAÇÃO DE GENES DIFERENCIALMENTE EXPRESSOS EM GLIOBLASTOMA E SUA RELAÇÃO NAS VIAS DO SISTEMA IMUNOLÓGICO Santa Maria, RS 2016." Centro Universitário Franciscano, 2016. http://www.tede.universidadefranciscana.edu.br:8080/handle/UFN-BDTD/546.
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Microarrays are instruments for measurement and analysis of several genes simultaneously, one of its uses is the verification of distinguishing gene expression in diseases. This work aims to verify the distinction between the expression of proteins in glioblastoma, using the data collected from the Gene Expression Omnibus database, because this cancer is characterized as of high incidence and it’s difficult to treat. After computational statistical analysis, it was found that the genes TNIP2, TOLLIP, IKBKB, PSMF1, RASGRF2, NEFL, DNM1, CDC42, YES1, C1S and PAK1, are differentially expressed in the pathways of the immune system, however, only the genes TNIP2, TOLLIP, IKBKB, are part of the NF-KB pathway, known to fight inflammation. The expectation of this work, and it´s future studies, hope to demonstrate different expressed genes in the immune system and thus help to better understand the development of the disease and its treatment, by nanoencapsulation of temozolimoda, a drug used along with radiotherapy.
Microarranjos são instrumentos para leituras e análise de vários genes simultaneamente, sendo uma de suas utilizações a verificação da distinção de expressão de genes em doenças. A partir disso, este trabalho busca verificar a distinção de expressão entre as proteínas de glioblastoma, por meio de dados recolhidos do banco de dados Gene Expression Omnibus, por caracterizar-se como um câncer de grande incidência e difícil tratamento. Na análise estatística computacional realizada, constatou-se que os genes TNIP2, TOLLIP, IKBKB, PSMF1, RASGRF2, NEFL, DNM1, CDC42, YES1, C1S e PAK1, encontram-se diferencialmente expressos nas vias do sistema imunológico, porém, somente os genes TNIP2, TOLLIP, IKBKB, fazem parte da via NF-KB, conhecida no combate à inflamação. Espera-se com esse trabalho, além de aprimorá-lo em estudos futuros, complementar os estudos nesta área, pois sua análise poderá demonstrar diferentes genes expressos nas vias do sistema imunológico, podendo, assim, auxiliar na melhor compreensão no desenvolvimento da doença, bem como, seu tratamento, por meio da nanoencapsulação do temozolimoda, medicamento utilizado juntamente com radioterapia.
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Silva, Cláudia Regina dos Santos. "Análise da expressão de genes envolvidos na resposta inflamatória em crianças com síndrome de Down." Faculdade de Medicina de São José do Rio Preto, 2015. http://hdl.handle.net/tede/286.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
ABSTRACT Introduction: Down syndrome (DS) is a genetic disorder caused by the presence of an extra copy of human chromosome 21 (HSA21) with an incidence of one in 660 live births. Individuals with DS show alterations of the immune system resulting in increased frequency of infections and autoimmune diseases. Studies show that some genes involved in the immune system present altered expression in individuals with DS, however, the molecular mechanisms by which trisomy 21 leads to the immune system disorders in DS remain poorly investigated. Objective: This study aimed to investigate the expression pattern of a specific set of genes involved in the immune system and inflammation process in children with DS and children without the syndrome (control group), to identify differences that may be related to clinical manifestations of the syndrome. Casuistic and Methods: In this study were included six children with DS and six children without the syndrome. The quantification of the gene expression was performed using TaqMan ® Array Plate Human Inflammation Kit, which enables the investigation of 92 inflammation-related genes and four reference genes by real-time polymerase chain reaction (qPCR). Results: Of the 92 genes analyzed, 20 genes showed differential expression in children DS; 12 overexpressed (PLA2G2D, CACNA1D, ALOX12, VCAM1, ICAM1, PLCD1, ADRB1, HTR3A, PDE4C, CASP1, PLA2G5 e PLCB4) and 8 underexpressed (LTA4H, BDKRB1, ADRB2, CD40LG, ITGAM, TNFRSF1B, ITGB1 e TBXAS1). After statistical correction for false discovery rate, only the genes BDKRB1 and LTA4H showed differential expression, both underexpressed. Conclusion: DS children show differential expression of genes, not located on chromosome 21, compared to children without DS. The altered expression of these genes, considering their functions in the inflammatory response, suggests an important role in DS pathogenesis.
RESUMO Introdução: A síndrome de Down (SD) é um distúrbio genético causado pela presença de uma cópia extra do cromossomo humano 21 (HSA 21) com uma incidência de um a cada 660 nascidos vivos. Indivíduos com SD apresentam alterações no sistema imunológico que resultam no aumento da frequência de infecções e doenças autoimunes. Estudos mostram que alguns genes envolvidos no sistema imunológico apresentam expressão alterada em indivíduos com SD, entretanto, os mecanismos moleculares pelos quais a trissomia do 21 leva aos distúrbios do sistema imunológico em SD permanecem pouco investigados. Objetivo: O presente trabalho teve como objetivo investigar o padrão de expressão de um conjunto específico de genes envolvidos no sistema imunológico e no processo inflamatório em crianças com SD e crianças sem a síndrome (grupo controle), visando identificar diferenças que possam estar relacionadas com manifestações clínicas da síndrome. Casuística e Métodos: Foram incluídas no estudo seis crianças com SD e seis crianças sem a síndrome. A quantificação da expressão gênica foi realizada com o kit TaqMan® Human Plate Inflammation Array, que permite a investigação de 92 genes relacionados com a inflamação e quatro genes de referência pelo método de reação em cadeia da polimerase quantitativa em tempo real (PCRq). Resultados: Dos 92 genes analisados, 20 genes apresentaram expressão diferencial em crianças com SD; 12 com expressão aumentada (PLA2G2D, CACNA1D, ALOX12, VCAM1, ICAM1, PLCD1, ADRB1, HTR3A, PDE4C, CASP1, PLA2G5 e PLCB4) e oito com expressão reduzida (LTA4H, BDKRB1, ADRB2, CD40LG, ITGAM, TNFRSF1B, ITGB1 e TBXAS1). Após correção estatística para múltiplos testes apenas os genes BDKRB1 e LTA4H apresentaram expressão diferencial, ambos com expressão reduzida. Conclusão: Crianças com SD apresentam expressão diferencial de genes, não localizados no cromossomo 21, em relação a crianças sem a síndrome. A expressão alterada desses genes, considerando suas funções na resposta inflamatória, sugere um papel relevante na patogênese da SD.
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Shater, A. F. "Investigation of DNA variation in genes of the immune system in wild populations of Apodemus sylvaticus in relation to infection by Toxoplasma gondii and helminth parasites." Thesis, University of Salford, 2017. http://usir.salford.ac.uk/44600/.
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The aims of this study are to investigate DNA sequence variation in immune genes from Apodemus sylvaticus in relation to parasite infection. The purpose is to investigate the hypothesis that immune gene variation can influence parasite infection. Evidence from other studies, such as infection of wild voles with Borrelia and cattle with bovine tuberculosis, has demonstrated that the DNA sequence (and therefore the protein sequence) of toll-like receptors (TLRs) is correlated with infection status. Recent laboratory studies on mice showed that the genes for TLR11 or TLR12 are essential for recognition of the parasite Toxoplasma gondii. Furthermore, the NLRP1b gene, a key component in regulating inflammation during infection, her been found in laboratory studies to be responsible for resistance of the mice against toxoplasmosis. Also, it is located at the Toxo1 locus which has been shown to be a key host locus for controlling Toxoplasma parasite proliferation and recent studies on inbred mice confirm that NLRP1b is the main gene that is responsible for this control. But little is known of the role of these innate immune system genes in natural populations. The purpose of this study is to investigate gene diversity in relation to parasite infection in wild rodent populations. A recent study in our laboratory resulted in 126 wild wood mice (Apodemus sylvaticus) being tested for T. gondii infection and other helminth parasites. This provides a topical opportunity to investigate DNA polymorphisms in NLRP1 and TLRs that could be associated with infection. In a study which investigated polymorphisms in relation to TLR11 and TLR 12, several relations were obtained but only one of them is significant which is the relationship between Syphacea infection with H2 and non H2 haplotype. At the start of the project no sequence was available for the NLRP1b gene from A. sylvaticus. Using Clustal alignment of DNA sequences from Mus musculus and other rodents, several combinations of PCR primer pairs were designed and tested for the amplification of parts of this gene from A. sylvaticus. The amplification is complex due to the arrangement of exons and introns, but successful sequences have been obtained for Exon 3 part 2 and Exon 3 part 3 (approximately 450 base pairs) which covers the function region, called NACHT, from 80 mice. Polymorphisms were found at amino acid positions 15 and 22 of exon 3-2 and positions 11 and 36 of exon 3-3. Exon 3-2 amino acid polymorphism is either methionine or leucine at position 15 and glutamic acid or alanine at position 22. Exon 3-3 amino acid polymorphism is either histidine or leucine at position 16 and glutamic acid or lysine at position 36. The polymorphisms found in the NLRP1b gene were examined for any relationship to a broad range of nematode parasites. One of the exon 3-2 haplotypes (H1/H2) shows a significant association with different nematodes and two haplotypes (H2/H3 and H4/H4) have a significant association with Toxoplasma gondii in respect for different helminth parasites. Furthermore, three of the exon 3-3 haplotypes (H1/H4, H4/H4 and H3/H3) show a significant association with different nematodes and one haplotype (H4/H4) has a significant association with Toxoplasma gondii. In addition, one haplotype of exon 3-3 which is H2/H2 showed a significant association with parasitic infection status (negative or multiple parasites). Also, the homozygosity and heterozygosity of the SNPs were investigated. For exon 3-2, the homozygosity of the first SNPs locus showed significant association with Toxoplasma gondii. For exon 3-3, the homozygosity of the first SNPs locus, and the second SNPs locus when analysed separately show significant association with Toxoplasma gondii. But, when analysed together, the heterozygosity of both SNPs locus showed significant association with Toxoplasma gondii in respect for different helminth parasites. In this study, DNA sequence variation was found in the immune genes (TLR11, 12 and NLRP1b) natural populations of wood mice. There was an association between some haplotypes and parasite infection. This provides evidence in support of the hypothesis that variation in immune gene sequences can influence parasite infection. Future studies should be aimed at identifying the detailed interactions between parasites and host immune genes in natural populations of wild animals.
Books on the topic "Immune system genes"
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Fox, C. Fred, Eli E. Sercarz, and Alan R. Williamson. Immune System: Genes, Receptors, Signals. Elsevier Science & Technology Books, 2013.
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Cantor, Harvey, Leonard Chess, and Eli E. Sercarz. Regulation of the Immune System. Wiley & Sons, Incorporated, John, 1985.
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Radtke, Freddy. Notch Regulation of the Immune System. Springer London, Limited, 2012.
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Radtke, Freddy. Notch Regulation of the Immune System. Springer Berlin / Heidelberg, 2014.
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Notch Regulation Of The Immune System. Springer, 2012.
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(Editor), Y. Becker, and Gholamreza Darai (Editor), eds. Molecular Evolution of Viruses - Past and Present: Evolution of Viruses by Acquisition of Cellular RNA and DNA (VIRUS GENES). Springer, 2007.
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Becker, Yechiel. Molecular Evolution of Viruses - Past and Present: Evolution Of Viruses By Acquisition Of Cellular Rna And Dna. Springer, 2012.
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Yechiel, Becker, and Darai Gholamreza, eds. Molecular evolution of viruses-past and present: Evolution of viruses by acquisition of cellular RNA and DNA. Boston: Kluwer Academic Publishers, 2000.
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Becker, Yechiel. Molecular Evolution of Viruses - Past and Present. Springer, 2011.
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Becker, Yechiel, and Gholamreza Darai. Molecular Evolution of Viruses -- Past and Present: Evolution of Viruses by Acquisition of Cellular RNA and DNA. Springer London, Limited, 2012.
Find full textBook chapters on the topic "Immune system genes"
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Beermann, Christopher. "Immunogenetics: Influences of Food Components on the Expression of Immune-Related Genes." In Food and the Immune System, 177–209. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11523-3_7.
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Ohno, Susumu. "Of Words, Genes and Music." In The Semiotics of Cellular Communication in the Immune System, 131–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73145-7_12.
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Ayliffe, Michael, Ming Luo, Justin Faris, and Evans Lagudah. "Disease Resistance." In Wheat Improvement, 341–60. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-90673-3_19.
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AbstractWheat plants are infected by diverse pathogens of economic significance. They include biotrophic pathogens like mildews and rusts that require living plant cells to proliferate. By contrast necrotrophic pathogens that cause diseases such as tan spot, Septoria nodurum blotch and spot blotch require dead or dying cells to acquire nutrients. Pioneering studies in the flax plant-flax rust pathosystem led to the ‘gene-for-gene’ hypothesis which posits that a resistance gene product in the host plant recognizes a corresponding pathogen gene product, resulting in disease resistance. In contrast, necrotrophic wheat pathosystems have an ‘inverse gene-for-gene’ system whereby recognition of a necrotrophic fungal product by a dominant host gene product causes disease susceptibility, and the lack of recognition of this pathogen molecule leads to resistance. More than 300 resistance/susceptibility genes have been identified genetically in wheat and of those cloned the majority encode nucleotide binding, leucine rich repeat immune receptors. Other resistance gene types are also present in wheat, in particular adult plant resistance genes. Advances in mutational genomics and the wheat pan-genome are accelerating causative disease resistance/susceptibility gene discovery. This has enabled multiple disease resistance genes to be engineered as a transgenic gene stack for developing more durable disease resistance in wheat.
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Hansen, J. D., and J. F. McBlane. "Recombination-Activating Genes, Transposition, and the Lymphoid-Specific Combinatorial Immune System: A Common Evolutionary Connection." In Current Topics in Microbiology and Immunology, 111–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59674-2_6.
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Johnson, K. A., J. J. Michal, G. E. Carstens, A. N. Hafla, and T. D. A. Forbes. "Differential expression of innate immune system genes in liver of beef cattle with divergent phenotypes for RFI." In Energy and protein metabolism and nutrition in sustainable animal production, 371–72. Wageningen: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-781-3_130.
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Kastenschmidt, Jenna M., Ali H. Mannaa, Karissa J. Muñoz, and S. Armando Villalta. "Immune System Regulation of Muscle Injury and Disease." In Muscle Gene Therapy, 121–39. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03095-7_7.
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Mahajan, Vineet, Shruti Saptarshi, and Yashwant Pathak. "Herpesvirus microRNAs for Use in Gene Therapy Immune-Evasion Strategies." In Gene Delivery Systems, 129–38. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003186083-10.
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Faldu, Khushboo, Sakshi Gurbani, and Jigna Shah. "Clinical Applications of Gene Therapy for Immuno-Deficiencies." In Gene Delivery Systems, 195–206. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003186083-14.
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Gillet, Laurent, and Alain Vanderplasschen. "Viral Subversion of the Immune System." In Applications of Gene-Based Technologies for Improving Animal Production and Health in Developing Countries, 257–91. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3312-5_20.
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Pampusch, Mary S., Mark A. Osinski, Janet R. Serie, Michael P. Murtaugh, and David R. Brown. "Opioid Receptor Gene Expression in the Porcine Immune System." In Advances in Experimental Medicine and Biology, 59–65. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5347-2_7.
Full textConference papers on the topic "Immune system genes"
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Božić, Dragica, Katarina Živančević, Katarina ,. Baralić, Dragana Javorac, Aleksandra Buha Đorđević, Evica Antonijević Miljaković, Đurđica Marić, et al. "APPLYING „IN SILICO“ TOXICOGENOMIC DATA MINING TO PREDICT MOLECULAR MECHANISMS AND PATHWAYS AGAINST CARCINOMA: IMMUNOMODULATOR SULFORAPHANE AS A CASE STUDY." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.470b.
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The aim of this study was to predict the molecular mechanisms and pathways of immunomodulator sulforaphane (SFN) against carcinoma using in silico toxicogenomic data mining. Three key tools applied in our analysis were Comparative Toxicogenomics Database (CTD; http://CTD.mdibl. org), ToppGene Suite portal (https://toppgene.cchmc.org) and Reactome Knowledgebase (https://reactome.org). Sulforaphane interacted with a total of 1896, among which NFE2L2, NQO1, HMOX1, GCLC, TXNRD1, IL1B, IFNG, AGT, KEAP1, and CASP3 had the highest number of interactions. In the CTD, there were direct evidences that SFN interacts with a total of 169 genes to express a therapeutic effect against different types of cancer such as: hepatocellular carcinoma (113), colorectal neoplasms (67), uterine cervical neoplasms (10), and adenomatous polyposis coli (4). This set of genes was further uploaded into the Gene Mania software, ToppGene Suite portal, and Reactome Knowledgebase, which confirmed that molecular functions, biological processes and pathways of SFN-affected genes were mostly related to oxidoreductase activity, regulation of immune system, and apoptosis. In conclusion, we may suggest that SFN interacts with host immunity to enhance the eradication of tumor cells mainly by inducing immune-response and stimulating apoptotic process of tumor cells. Moreover, its antioxidative activity could contribute to better anti-cancerogenic effects.
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Suprun, E., S. Suprun, E. Nagovicina, G. Evseeva, O. Lebed'ko, R. Telepneva, and O. Galyant. "Covid-19 and Some Polymorphisms in Genes of Signaling Molecules of the Immune System." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1166.
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Kamareddine, Layla, Hoda Najjar, Abeer Mohbeddin, Nawar Haj Ahmed, and Paula Watnick. "Between Immunity, Metabolism, and Development: A story of a Fly Gut!" In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0141.
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In addition to its role in initiating immune response in the body, the innate immune system seems to also play a critical role in maintaining homeostatic balance in the gut epithelium. Our recent studies in the Drosophila melanogaster fruit fly model suggest that different innate immune pathways contribute to this homeostatic balance through activating the transcription of genes encoding antimicrobial peptides. We provide evidence that several metabolic parameters are altered in immune deficient flies. We also highlight a role of the gut flora, particularly through its short chain fatty acid, in contributing to this metabolic balance. Interestingly, our data suggest that impaired immunity and metabolic alteration, in turn, exhibit an effect on host development. Collectively, these findings provide evidence that innate immune pathways not only provide the first line of defense against infection but also contribute to host metabolism and development.
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Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.
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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
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Suprun, E., E. Nagovitsina, O. Lebedko, and S. Suprun. "Genes Polymorphisms of Signalling Molecules of the Immune System as a Factor of Uncontrolled Bronchial Asthma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3054.
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Супрун, Стефания, Stefaniya Suprun, Елена Наговицына, E. Nagovitsyna, Ольга Лебедько, and Olga Lebedko. "Polymorphisms of genes signal molecules of the immune system as a factor of uncontrolled asthma bronchial." In The VIII Congress of Pulmonologists of Siberia and the Far East with international participation. Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2019. http://dx.doi.org/10.12737/conferencearticle_5ce51ce1e6ce31.09763500.
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Kornev, A. A., V. V. Vysochinskaya, N. A. Knyazev, A. K. Emel'yanov, and A. A. Bogdanov. "Transfection of human peripheral blood T-lymphocytes with synthetic small interfering RNAs: selection of an effective technique." In Global science. Development and novelty. L-Journal, 2020. http://dx.doi.org/10.18411/gsdn-25-12-2020-04.
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It has been shown that the state of the human immune system and its activity determines the development, course and prognosis of many oncological diseases. To date, various immunotherapeutic approaches have been developed, of which the most promising is adoptive cell therapy (ACT). An increase in the effectiveness of this type of therapy could be achieved by using synthetic small interfering RNAs (siRNAs) to suppress the expression of key immune checkpoint (ICI) genes (PD1, CTL4) in T-lymphocytes, which are involved in cellular immunosuppression. However, there is a problem of selecting an effective method for delivering such siRNAs to T-lymphocytes. In the present study, we developed a synthetic siRNA specific to the mRNA sequence of the PD1 gene and evaluated the efficiency of its delivery to activated human T-lymphocytes using chemically modified siRNA, histone H1, – 18 – Global science. Development and novelty and the liposomal agent HiperFect. Ex vivo activated T-lymphocytes from healthy donors were used. The efficiency of siRNA transfection into cells and its confirmation was assessed using flow cytofluorometry and confocal microscopy. As a result of the study, a high (51%) efficiency of transfection into these cells using chemically modified "self-delivering" siRNA was shown. For other methods of delivery of miRNA to T-lymphocytes, low efficiency is shown. Thus, our data suggest that of the three approaches used in this work for miRNAs delivery to activated T-lymphocytes, the most effective is the use of “self-delivering” chemically modified cholesterol miRNA.
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Anandakrishnan, Ramu, Robin T. Varghese, Nicholas A. Kinney, and Harold R. Garner. "Abstract PO022: Somatic mutations in tumor infiltrating lymphocytes can affect the expression of immune system genes in the tumor microenvironment." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po022.
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Campbell, MJ, J. Zhu, C. Yau, R. Muhktar, O. Nseyo, CC Benz, and LJ Esserman. "Abstract P5-04-01: Expression of Genes Associated with the Innate Immune System and Response to Neoadjuvant Chemotherapy in Breast Cancer." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p5-04-01.
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Jurišić, Vladimir. "POSSIBILITIES OF CYTOKINE DETERMINATION AND THEIR ANALYSIS IN VARIOUS TISSUES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.089j.
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Cytokines are small proteins that participate in many interactions between cells of the immune system as well as between many tissue cells including tumors. Currently, there is no universal classification of cytokines and they can be analyzed based on the cells that produce them or based on the type of activity. Cytokines have been studied for many years in medicine firstly in cancer patients in serum, but also in many other diseases including inflammation or other autoimmune diseases or other pathological conditions. Cytokines are still being discovered, and for many of them the structure, biological action and genes responsible for their regulation have already been determined. Bearing in mind that the development of technology has been developing enormously in the last period and those new methods of cytokine determination in various fluids and micro-concentrations are available to us. Here, the aim is to focus on the specific possibilities of determination and analysis of cytokine values in different tissues including cell culture supernatants, in individual cells as well as their genetic regulation. However, to understand their complex action in biological systems, including the pleiotropic effect of cytokines showing some time the overlap in the actions various models of analysis and interpretation of the obtained data are recommended today. This is especially complex and problematic in recent times of understanding the cytokine gene regulation and especially the possibility of their prediction. To resolve these problems, numerous databases have been created on the previously available experimental data, although their connection is not yet very clear. In addition, using integration of data, it is expected predict some models and systems in a specific situation, although it is still very difficult. So, aims are predict values in definitive situation and compare with some standards. Therefore, new methods of interpretation and new programs for analysis have been created. We expect that based on the new possibilities of analysis, better results will be achieved and that the role of these mediators for individual or personalized diagnosis or therapy in biomedicine will be determined.
Reports on the topic "Immune system genes"
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Cahaner, Avigdor, Susan J. Lamont, E. Dan Heller, and Jossi Hillel. Molecular Genetic Dissection of Complex Immunocompetence Traits in Broilers. United States Department of Agriculture, August 2003. http://dx.doi.org/10.32747/2003.7586461.bard.
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Objectives: (1) Evaluate Immunocompetence-OTL-containing Chromosomal Regions (ICRs), marked by microsatellites or candidate genes, for magnitude of direct effect and for contribution to relationships among multiple immunocompetence, disease-resistance, and growth traits, in order to estimate epistatic and pleiotropic effects and to predict the potential breeding applications of such markers. (2) Evaluate the interaction of the ICRs with genetic backgrounds from multiple sources and of multiple levels of genetic variation, in order to predict the general applicability of molecular genetic markers across widely varied populations. Background: Diseases cause substantial economic losses to animal producers. Emerging pathogens, vaccine failures and intense management systems increase the impact of diseases on animal production. Moreover, zoonotic pathogens are a threat to human food safety when microbiological contamination of animal products occurs. Consumers are increasingly concerned about drug residues and antibiotic- resistant pathogens derived from animal products. The project used contemporary scientific technologies to investigate the genetics of chicken resistance to infectious disease. Genetic enhancement of the innate resistance of chicken populations provides a sustainable and ecologically sound approach to reduce microbial loads in agricultural populations. In turn, animals will be produced more efficiently with less need for drug treatment and will pose less of a potential food-safety hazard. Major achievements, conclusions and implications:. The PI and co-PIs had developed a refined research plan, aiming at the original but more focused objectives, that could be well-accomplished with the reduced awarded support. The successful conduct of that research over the past four years has yielded substantial new information about the genes and genetic markers that are associated with response to two important poultry pathogens, Salmonella enteritidis (SE) and Escherichia coli (EC), about variation of immunocompetence genes in poultry, about relationships of traits of immune response and production, and about interaction of genes with environment and with other genes and genetic background. The current BARD work has generated a base of knowledge and expertise regarding the genetic variation underlying the traits of immunocompetence and disease resistance. In addition, unique genetic resource populations of chickens have been established in the course of the current project, and they are essential for continued projects. The US laboratory has made considerable progress in studies of the genetics of resistance to SE. Microsatellite-marked chromosomal regions and several specific genes were linked to SE vaccine response or bacterial burden and the important phenomenon of gene interaction was identified in this system. In total, these studies demonstrate the role of genetics in SE response, the utility of the existing resource population, and the expertise of the research group in conducting such experiments. The Israeli laboratories had showed that the lines developed by selection for high or low level of antibody (Ab) response to EC differ similarly in Ab response to several other viral and bacterial pathogens, indicating the existence of a genetic control of general capacity of Ab response in young broilers. It was also found that the 10w-Ab line has developed, possibly via compensatory "natural" selection, higher cellular immune response. At the DNA levels, markers supposedly linked to immune response were identified, as well as SNP in the MHC, a candidate gene responsible for genetic differences in immunocompetence of chickens.
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of Pest Control by Insect Immunosuppression. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592113.bard.
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The restricted host range of many baculoviruses, highly pathogenic to Lepidoptera and non-pathogenic to mammals, limits their use to single or few closely related Lepidopteran species and is an obstacle to extending their implementation for pest control. The insect immune response is a major determinant of the ability of an insect pathogen to efficiently multiply and propagate. We have developed an original model system to study the Lepidopteran antiviral immune response based on Spodoptera littoralis resistance to AcMNPV (Autographa californica multiple nucleopolyhedrovirus) infection and the fascinating immunosuppressive activity of polydnaviruses .Our aim is to elucidate the mechanisms through which the immunosuppressive insect polydnaviruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication. In this study we : 1- Assessed the extent to which and the mechanisms whereby the immunosuppressive Campoletis sonorensis polydnavirus (CsV) or its genes enhanced replication of a well-characterized pathogenic baculovirus AcMNPV, in polydnavirus-immunosuppressedH. zea and S. littoralis insects and S. littoralis cells, hosts that are mildly or non-permissive to AcMNPV. 2- Identified CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). We showed that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen, the baculovirus AcMNPV, to infect the pest. 3. For the first time two PDV-specific genes of the vankyrin and cystein rich-motif families involved in immunosuppression of the host, namely Pvank1 and Hv1.1 respectively, enhanced the efficacy of an insect pathogen toward a semipermissive pest. 4. Pvank1 inhibits apoptosis of Spodopteran cells elucidating one functional aspect of PDVvankyrins. 5. That Pvank-1 and Hv1.1 do not show cooperative effect in S. littoralis when co-expressed during AcMNPV infection. Our results pave the way to developing novel means for pest control, including baculoviruses, that rely upon suppressing host immune systems by strategically weakening insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence. Also, we expect that the above result will help to develop systems for enhanced insect control that may ultimately help to reduce transmission of insect vectored diseases of humans, animals and plants as well as provide mechanisms for suppression of insect populations that damage crop plants by direct feeding.
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Shpigel, Nahum Y., Ynte Schukken, and Ilan Rosenshine. Identification of genes involved in virulence of Escherichia coli mastitis by signature tagged mutagenesis. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699853.bard.
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Mastitis, an inflammatory response of the mammary tissue to invading pathogenic bacteria, is the largest health problem in the dairy industry and is responsible for multibillion dollar economic losses. E. coli are a leading cause of acute mastitis in dairy animals worldwide and certainly in Israel and North America. The species E. coli comprises a highly heterogeneous group of pathogens, some of which are commensal residents of the gut, infecting the mammary gland after contamination of the teat skin from the environment. As compared to other gut microflora, mammary pathogenic E. coli (MPEC) may have undergone evolutionary adaptations that improve their fitness for colonization of the unique and varied environmental niches found within the mammary gland. These niches include competing microbes already present or accompanying the new colonizer, soluble and cellular antimicrobials in milk, and the innate immune response elicited by mammary cells and recruited immune cells. However, to date, no specific virulence factors have been identified in E. coli isolates associated with mastitis. The original overall research objective of this application was to develop a genome-wide, transposon-tagged mutant collection of MPEC strain P4 and to use this technology to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. In the course of the project we decided to take an alternative genome-wide approach and to use whole genomes bioinformatics analysis. Using genome sequencing and analysis of six MPEC strains, our studies have shown that type VI secretion system (T6SS) gene clusters were present in all these strains. Furthermore, using unbiased screening of MPEC strains for reduced colonization, fitness and virulence in the murine mastitis model, we have identified in MPEC P4-NR a new pathogenicity island (PAI-1) encoding the core components of T6SS and its hallmark effectors Hcp, VgrG and Rhs. Next, we have shown that specific deletions of T6SS genes reduced colonization, fitness and virulence in lactating mouse mammary glands. Our long-term goal is to understand the molecular mechanisms of host-pathogen interactions in the mammary gland and to relate these mechanisms to disease processes and pathogenesis. We have been able to achieve our research objectives to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. The project elucidated a new basic concept in host pathogen interaction of MPEC, which for the best of our knowledge was never described or investigated before. This research will help us to shed new light on principles behind the infection strategy of MPEC. The new targets now enable prevalence and epidemiology studies of T6SS in field strains of MPEC which might unveil new geographic, management and ecological risk factors. These will contribute to development of new approaches to treat and prevent mastitis by MPEC and perhaps other mammary pathogens. The use of antibiotics in farm animals and specifically to treat mastitis is gradually precluded and thus new treatment and prevention strategies are needed. Effective mastitis vaccines are currently not available, structural components and effectors of T6SS might be new targets for the development of novel vaccines and therapeutics.
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Yogev, David, Ricardo Rosenbusch, Sharon Levisohn, and Eitan Rapoport. Molecular Pathogenesis of Mycoplasma bovis and Mycoplasma agalactiae and its Application in Diagnosis and Control. United States Department of Agriculture, April 2000. http://dx.doi.org/10.32747/2000.7573073.bard.
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Mycoplasma bovis and M. agalactiae are two phylogenetically related mycoplasmas which cause economically significant diseases in their respective bovine or small ruminant hosts. These organisms cause persistent asymptomatic infections that can result in severe outbreaks upon introduction of carrier animals into susceptible herds. Little is known about the mechanisms underlying mycoplasma-host interaction, variation in virulence, or of the factors enabling avoidance of the host immune system. In recent years it has become apparent that the ability of pathogenic microorganisms to rapidly alter surface antigenic structures and to fine tune their antigenicity, a phenomena called antigenic variation, is one of the most effective strategies used to escape immune destruction and to establish chronic infections. Our discovery of a novel genetic system, mediating antigenic variation in M. bovis (vsp) as well as in M. agalactiae (avg) served as a starting point for our proposal which included the following objectives: (i) Molecular and functional characterization of the variable surface lipoproteins (Vsp) system of M. bovis and comparison with the Vsp-counterpart in M. agalactiae (ii) Determination of the role of Vsp proteins in the survival of M. bovis when confronted by host defense factors, (iii) Assessment of Vsp-based genetic and antigenic typing of M. bovis and M. agalactiae for epidemiology of infection and (iv) Improvement of diagnostic tests for M. bovis and M. agalactiae based on the vsp-and vsp-analogous systems. We have carried out an extensive molecular characterization of the vsp system and unravelled the precise molecular mechanism responsible for the generation of surface antigenic variation in M. bovis. Our data clearly demonstrated that the two pathogenic mycoplasma species possess large gene families encoding variable lipoprotein antigens that apparently play an important role in immune evasion and in pathogen-host interaction during infection. Phase variable production of these antigens was found to be mediated by a novel molecular mechanism utilizing double site-specific DNA inversions via an intermediate vsp configuration. Studies in model systems indicate that phase variation of VspA is relevant in interaction between M. bovis and macrophages or monocytes, a crucial stage in pathogenesis. Using an ELISA test with captured VspA as an antigen, phase variation was shown to occur in vivo and under field conditions. Genomic rearrangements in the avg gene family of M. agalactiae were shown to occur in vivo and may well have a role in evasion of host defences and establishment of chronic infection. An epidemiological study indicated that patterns of vsp-related antigenic variation diverge rapidly in an M. bovis infected herd. Marked divergence was also found with avg-based genomic typing of M. agalactiae in chronically infected sheep. However, avg-genomic fingerprints were found to be relatively homogeneous in different animals during acute stages of an outbreak of Contagious Agalactiae, and differ between unrelated outbreaks. These data support the concept of vsp-based genomic typing but indicate the necessity for further refinement of the methodology. The molecular knowledge on these surface antigens and their encoding genes provides the basis for generating specific recombinant tools and serological methods for serodiagnosis and epidemiological purposes. Utilization of these methods in the field may allow differentiating acutely infected herds from chronic herds and disease-free herds. In addition the highly immunogenic nature of these lipoproteins may facilitate the design of protective vaccine against mycoplasma infections.
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Chejanovsky, Nor, and Suzanne M. Thiem. Isolation of Baculoviruses with Expanded Spectrum of Action against Lepidopteran Pests. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7586457.bard.
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Our long-term goal is to learn to control (expand and restrict) the host range of baculoviruses. In this project our aim was to expand the host range of the prototype baculovirus Autographa cali/arnica nuclear polyhedrosis virus (AcMNPV) towards American and Israeli pests. To achieve this objective we studied AcMNPV infection in the non-permissive hosts L. dispar and s. littoralis (Ld652Y and SL2 cells, respectively) as a model system and the major barriers to viral replication. We isolated recombinant baculoviruses with expanded infectivity towards L. dispar and S. littoralis and tested their infectivity towards other Lepidopteran pests. The restricted host range displayed by baculoviruses constitutes an obstacle to their further implementation in the control of diverse Lepidopteran pests, increasing the development costs. Our work points out that cellular defenses are major role blocks to AcMNPV replication in non- and semi-permissive hosts. Therefore a major determinant ofbaculovirus host range is the ability of the virus to effectively counter cellular defenses of host cells. This is exemplified by our findings showing tliat expressing the viral gene Ldhrf-l overcomes global translation arrest in AcMNPV -infected Ld652Y cells. Our data suggests that Ld652Y cells have two anti-viral defense pathways, because they are subject to global translation arrest when infected with AcMNPV carrying a baculovirus apoptotic suppressor (e.g., wild type AcMNPV carryingp35, or recombinant AcMNPV carrying Opiap, Cpiap. or p49 genes) but apoptose when infected with AcMNPV-Iacking a functional apoptotic suppressor. We have yet to elucidate how hrf-l precludes the translation arrest mechanism(s) in AcMNPV-infected Ld652Y cells. Ribosomal profiles of AcMNPV infected Ld652Y cells suggested that translation initiation is a major control point, but we were unable to rule-out a contribution from a block in translation elongation. Phosphorylation of eIF-2a did not appear to playa role in AcMNPV -induced translation arrest. Mutagenesis studies ofhrf-l suggest that a highly acidic domain plays a role in precluding translation arrest. Our findings indicate that translation arrest may be linked to apoptosis either through common sensors of virus infection or as a consequence of late events in the virus life-cycle that occur only if apoptosis is suppressed. ~ AcMNPV replicates poorly in SL2 cells and induces apoptosis. Our studies in AcMNPV - infected SL2ceils led us to conclude that the steady-state levels of lEI (product of the iel gene, major AcMNPV -transactivator and multifunctional protein) relative to those of the immediate early viral protein lEO, playa critical role in regulating the viral infection. By increasing the IEl\IEO ratio we achieved AcMNPV replication in S. littoralis and we were able to isolate recombinant AcMNPV s that replicated efficiently in S. lifforalis cells and larvae. Our data that indicated that AcMNPV - infection may be regulated by an interaction between IE 1 and lED (of previously unknown function). Indeed, we showed that IE 1 associates with lED by using protein "pull down" and immunoprecipitation approaches High steady state levels of "functional" IE 1 resulted in increased expression of the apoptosis suppressor p35 facilitating AcMNPV -replication in SL2 cells. Finally, we determined that lED accelerates the viral infection in AcMNPV -permissive cells. Our results show that expressing viral genes that are able to overcome the insect-pest defense system enable to expand baculovirus host range. Scientifically, this project highlights the need to further study the anti-viral defenses of invertebrates not only to maximi~e the possibilities for manipulating baculovirus genomes, but to better understand the evolutionary underpinnings of the immune systems of vertebrates towards virus infection.
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Fluhr, Robert, and Maor Bar-Peled. Novel Lectin Controls Wound-responses in Arabidopsis. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697123.bard.
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Innate immune responses in animals and plants involve receptors that recognize microbe-associated molecules. In plants, one set of this defense system is characterized by large families of TIR–nucleotide binding site–leucine-rich repeat (TIR-NBS-LRR) resistance genes. The direct interaction between plant proteins harboring the TIR domain with proteins that transmit and facilitate a signaling pathway has yet to be shown. The Arabidopsis genome encodes TIR-domain containing genes that lack NBS and LRR whose functions are unknown. Here we investigated the functional role of such protein, TLW1 (TIR LECTIN WOUNDRESPONSIVE1). The TLW1 gene encodes a protein with two domains: a TIR domain linked to a lectin-containing domain. Our specific aim in this proposal was to examine the ramifications of the TL1-glycan interaction by; A) The functional characterization of TL1 activity in the context of plant wound response and B) Examine the hypothesis that wounding induced specific polysaccharides and examine them as candidates for TL-1 interactive glycan compounds. The Weizmann group showed TLW1 transcripts are rapidly induced by wounding in a JA-independent pathway and T-DNA-tagged tlw1 mutants that lack TLW1 transcripts, fail to initiate the full systemic wound response. Transcriptome methodology analysis was set up and transcriptome analyses indicates a two-fold reduced level of JA-responsive but not JA-independent transcripts. The TIR domain of TLW1 was found to interact directly with the KAT2/PED1 gene product responsible for the final b-oxidation steps in peroxisomal-basedJA biosynthesis. To identify potential binding target(s) of TL1 in plant wound response, the CCRC group first expressed recombinant TL1 in bacterial cells and optimized conditions for the protein expression. TL1 was most highly expressed in ArcticExpress cell line. Different types of extraction buffers and extraction methods were used to prepare plant extracts for TL1 binding assay. Optimized condition for glycan labeling was determined, and 2-aminobenzamide was used to label plant extracts. Sensitivity of MALDI and LC-MS using standard glycans. THAP (2,4,6- Trihydroxyacetophenone) showed minimal background peaks at positive mode of MALDI, however, it was insensitive with a minimum detection level of 100 ng. Using LC-MS, sensitivity was highly increased enough to detect 30 pmol concentration. However, patterns of total glycans displayed no significant difference between different extraction conditions when samples were separated with Dionex ICS-2000 ion chromatography system. Transgenic plants over-expressing lectin domains were generated to obtain active lectin domain in plant cells. Insertion of the overexpression construct into the plant genome was confirmed by antibiotic selection and genomic DNA PCR. However, RT-PCR analysis was not able to detect increased level of the transcripts. Binding ability of azelaic acid to recombinant TL1. Azelaic acid was detected in GST-TL1 elution fraction, however, DHB matrix has the same mass in background signals, which needs to be further tested on other matrices. The major findings showed the importance of TLW1 in regulating wound response. The findings demonstrate completely novel and unexpected TIR domain interactions and reveal a control nexus and mechanism that contributes to the propagation of wound responses in Arabidopsis. The implications are to our understanding of the function of TIR domains and to the notion that early molecular events occur systemically within minutes of a plant sustaining a wound. A WEB site (http://genome.weizmann.ac.il/hormonometer/) was set up that enables scientists to interact with a collated plant hormone database.
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Sessa, Guido, and Gregory Martin. role of FLS3 and BSK830 in pattern-triggered immunity in tomato. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604270.bard.
Full textAbstract:
Pattern-recognition receptors (PRRs) located on the plant cell surface initiate immune responses by perceiving conserved pathogen molecules known as pathogen-associated molecular patterns (PAMPs). PRRs typically function in multiprotein complexes that include transmembrane and cytoplasmickinases and contribute to the initiation and signaling of pattern-triggered immunity (PTI). An important challenge is to identify molecular components of PRR complexes and downstream signaling pathways, and to understand the molecular mechanisms that mediate their function. In research activities supported by BARD-4931, we studied the role of the FLAGELLIN SENSING 3 (FLS3) PRR in the response of tomato leaves to flagellin-derivedPAMPs and PTI. In addition, we investigated molecular properties of the tomato brassinosteroid signaling kinase 830 (BSK830) that physically interacts with FLS3 and is a candidate for acting in the FLS3 signaling pathway. Our investigation refers to the proposal original objectives that were to: 1) Investigate the role of FLS3 and its interacting proteins in PTI; 2) Investigate the role of BSK830 in PTI; 3) Examine molecular and phosphorylation dynamics of the FLS3-BSK830 interaction; 4) Examine the possible interaction of FLS3 and BSK830 with Pstand Xcveffectors. We used CRISPR/Cas9 techniques to develop plants carrying single or combined mutations in the FLS3 gene and in the paralogsFLS2.1 and FLS2.2 genes, which encode the receptor FLAGELLIN SENSING2 (FLS2), and analyzed their function in PTI. Domain swapping analysis of the FLS2 and FLS3 receptors revealed domains of the proteins responsible for PAMP detection and for the different ROS response initiated by flgII-28/FLS3 as compared to flg22/FLS2. In addition, in vitro kinase assays and point mutations analysis identified FLS2 and FLS3 domains required for kinase activity and ATP binding. In research activities on tomato BSK830, we found that it interacts with PRRs and with the co-receptor SERK3A and PAMP treatment affects part of these interactions. CRISPR/Cas9 bsk830 mutant plants displayed enhanced pathogen susceptibility and reduced ROS production upon PAMP treatment. In addition, BSK830 interacted with 8 Xanthomonastype III secreted effectors. Follow up analysis revealed that among these effectors XopAE is part of an operon, is translocated into plant cells, and displays E3 ubiquitinligase activity. Our investigation was also extended to other Arabidopsis and tomato BSK family members. Arabidopsis BSK5 localized to the plant cell periphery, interacted with receptor-like kinases, and it was phosphorylatedin vitro by the PEPR1 and EFRPRRs. bsk5 mutant plants displayed enhanced susceptibility to pathogens and were impaired in several, but not all, PAMP-induced responses. Conversely, BSK5 overexpression conferred enhanced disease resistance and caused stronger PTI responses. Genetic complementation suggested that proper localization, kinase activity, and phosphorylation by PRRs are critical for BSK5 function. BSK7 and BSK8 specifically interacted with the FLS2 PRR, their respective mutant plants were more susceptible to B. cinereaand displayed reduced flg22-induced responses. The tomato BSK Mai1 was found to interact with the M3KMAPKKK, which is involved in activation of cell death associated with effector-triggered immunity. Silencing of Mai1 in N. benthamianaplants compromised cell death induced by a specific class of immune receptors. In addition, co-expression of Mai1 and M3Kin leaves enhanced MAPKphosphorylation and cell death, suggesting that Mai1 acts as a molecular link between pathogen recognition and MAPK signaling. Finally, We identified the PP2C phosphatase Pic1 that acts as a negative regulator of PTI by interacting with and dephosphorylating the receptor-like cytoplasmickinase Pti1, which is a positive regulator of plant immunity. The results of this investigation shed new light on the molecular characteristics and interactions of components of the immune system of crop plants providing new knowledge and tools for development of novel strategies for disease control.
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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.
Full textAbstract:
The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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Gafni, Yedidya, Moshe Lapidot, and Vitaly Citovsky. Dual role of the TYLCV protein V2 in suppressing the host plant defense. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7597935.bard.
Full textAbstract:
TYLCV-Is is a major tomato pathogen, causing extensive crop losses in Israel and the U.S. We have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing. Intriguingly, the counter-defense function of V2 may not be limited to silencing suppression. Our recent data suggest that V2 interacts with the tomato CYP1 protease. CYP1 belongs to the family of papain-like cysteine proteases which participate in programmed cell death (PCD) involved in plant defense against pathogens. Based on these data we proposed a model for dual action of V2 in suppressing the host antiviral defense: V2 targets SGS3 for degradation and V2 inhibits CYP1 activity. To study this we proposed to tackle three specific objectives. I. Characterize the role of V2 in SGS3 proteasomal degradation ubiquitination, II. Study the effects of V2 on CYP1 maturation, enzymatic activity, and accumulation and, III. Analyze the effects of the CYP1-V2 interaction on TYLCV-Is infection. Here we describe results from our study that support our hypothesis: the involvement of the host's innate immune system—in this case, PCD—in plant defense against TYLCV-Is. Also, we use TYLCV-Is to discover the molecular pathway(s) by which this plant virus counters this defense. Towards the end of our study we discovered an interesting involvement of the C2 protein encoded by TYLCV-Is in inducing Hypersensitive Response in N. benthamianaplants which is not the case when the whole viral genome is introduced. This might lead to a better understanding of the multiple processes involved in the way TYLCV is overcoming the defense mechanisms of the host plant cell. In a parallel research supporting the main goal described, we also investigated Agrobacteriumtumefaciens-encoded F-box protein VirF. It has been proposed that VirF targets a host protein for the UPS-mediated degradation, very much the way TYLCV V2 does. In our study, we identified one such interactor, an Arabidopsistrihelix-domain transcription factor VFP3, and further show that its very close homolog VFP5 also interacted with VirF. Interestingly, interactions of VirF with either VFP3 or VFP5 did not activate the host UPS, suggesting that VirF might play other UPS-independent roles in bacterial infection. Another target for VirF is VFP4, a transcription factor that both VirF and its plant functional homolog VBF target to degradation by UPS. Using RNA-seqtranscriptome analysis we showed that VFP4 regulates numerous plant genes involved in disease response, including responses to viral and bacterial infections. Detailed analyses of some of these genes indicated their involvement in plant protection against Agrobacterium infection. Thus, Agrobacterium may facilitate its infection by utilizing the host cell UPS to destabilize transcriptional regulators of the host disease response machinery that limits the infection.
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Davidson, Irit, Hsing-Jien Kung, and Richard L. Witter. Molecular Interactions between Herpes and Retroviruses in Dually Infected Chickens and Turkeys. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7575275.bard.
Full textAbstract:
Tumors in commercial poultry are caused mainly by infection with avian herpes and retroviruses, the herpesvirus Marek's disease virus (MDV) and the retroviruses, reticuloendotheliosis (REV), lymphoid leukosis, subgroups A-I and J (ALV and ALV-J) in chickens, or Iymphoprolipherative disease (LPDV) in turkeys. Infection with one virus aggravates the clinical outcome of birds that are already infected by another oncogenic virus. As these viruses do not interfere for infection, MDV and one or more retroviruses can infect the same flock, the same bird and the same cell. While infecting the same cell, herpes and retroviruses might interact in at least three ways: a) Integration of retrovirus genomes, or genomic fragments (mainly the LTR) into MDV;b) alteration of LTR-driven expression of retroviral genes by MDV immediate- early genes, and c) by herpesvirus induced cellular transcriptional factors. The first type of molecular interaction have been demonstrated to happen efficiently in vitro by Dr. Kung, in cases multiple infection of cell cultures with MDV and REV or MDV and ALV. Moreover, Dr. Witter showed that an in vitro-created recombinant, RM1, had altered in vitro replication and in vivo biological properties. A more comprehensive characterization of RM1 was carried out in the present project. We sought to highlight whether events of such integrations occur also in the bird, in vivo. For that, we had first to determine the prevalence of dually-infected individual birds in commercial flocks, as no systematic survey has been yet reported. Surprisingly, about 25% of the commercial flocks infected with avian oncogenic viruses had a multiple virus infection and 5% of the total samples ana lysed had multiple virus sequences. Then, we aimed to evaluate and characterize biologically and molecularly the resulting recombinants, if formed, and to analyse the factors that affect these events (virus strains, type and age of birds and time interval between the infection with both viruses). The perception of retrovirus insertions into herpesviruses in vivo is not banal, as the in vivo and in vitro systems differ in the viral-target cells, lymphocytes or fibroblasts, in the MDV-replicative type, transforming or productive, and the immune system presence. We realized that previous methods employed to study in vitro created recombinant viruses were not adequate for the study of samples taken directly from the bird. Therefore, the Hot Spot-combined PCR was developed based on the molecularly known RM1 virus. Also, the PFGE that was used for tissue cultured-MDV separation was inefficient for separating MDV from organs, but useful with feather tips as a source of bird original MDV. Much attention was dedicated now to feathers, because if a recombinant virus would be formed in vivo, its biological significance would be evident by horizontal dissemination through the feathers. Major findings were: a) not only in vitro, but also in vivo MDV and retrovirus co-infections lead to LTR integrations into MDV. That was shown by the detection of chimeric molecules. These appeared in low quantities and as quasispecies, thus interfering with sequence analysis of cloned gel-purified chimeric molecules. Mainly inserts were located in the repeat long MDV fragments. In field birds chimeric molecules were detected at a lower frequency (2.5%) than in experimentally infected birds (30-50%). These could be transmitted experimentally to another birds by inoculation with chimeric molecules containing blood. Several types of chimeric molecules were formed, and same types were detected in birds infected by a second round. To reproduce viral integrations, in vivo infection trials were done with field inoculate that contained both viruses, but the chimeric molecule yield was undetectable.