Academic literature on the topic 'Immune response genes'
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Journal articles on the topic "Immune response genes"
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Du, Liping, Aize Kijlstra, and Peizeng Yang. "Immune Response Genes in Uveitis." Ocular Immunology and Inflammation 17, no. 4 (January 2009): 249–56. http://dx.doi.org/10.1080/09273940902999356.
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Cox, Diane W. "Genes of the immune response: disease associations." Genome 31, no. 2 (January 15, 1989): 1085–86. http://dx.doi.org/10.1139/g89-186.
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Béhar, Ghislaine, Yves Bourlet, Nancy Fréchin, François Guillemot, Rima Zoorob, and Charles Auffray. "Molecular analysis of chicken immune response genes." Biochimie 70, no. 7 (July 1988): 909–17. http://dx.doi.org/10.1016/0300-9084(88)90232-5.
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Hartman, Zachary, Xiao Yi Yang, Gangjun Lei, Andrea Amalfitano, Michael Morse, Herbert Kim Lyerly, and Tim Clay. "Modulation of adenoviral vector immune responses through the over-expression of immune adaptor and viral immuno-modulatory genes (48.17)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S77—S78. http://dx.doi.org/10.4049/jimmunol.178.supp.48.17.
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Abstract For the past two decades, adenoviral vector platforms have been used as both gene therapy vehicles and vaccine platforms in various human clinical trials. However, the use of these, as well as other viral vector platforms, has been tempered by the innate immune and adaptive immune responses elicited. Despite the development of advanced generation adenoviral vectors, the innate responses precipitated by these vectors have remained largely unchanged due to the particular nature of the viral capsid and infectious process. To more effectively use these vectors for different purposes, we constructed adenoviral vectors encoding overexpression cassettes for various TLR adaptors (MyD88 and TRIF), RIG-I pathway adaptor (MAVS), as well as immuno-modulatory viral genes (pp65) whose expression might accentuate or inhibit the innate immune response enabled by adenoviral infection. Our studies show that while all of these immuno-modulatory vectors were able to effectively enhance (TLR and MAVS vectors) or inhibit (pp65 vectors) the NF-kB and IFN-beta responses in vitro, only certain vectors were able to affect the adaptive responses elicited in vivo. While our findings show that vector manipulation can influence vector-specific innate and adaptive immune responses, they also offer evidence for the highly regulatory nature of the innate response, as evidenced by the limited impact of certain adaptor overexpression.
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Knapek, Katie J., Hanah M. Georges, Hana Van Campen, Jeanette V. Bishop, Helle Bielefeldt-Ohmann, Natalia P. Smirnova, and Thomas R. Hansen. "Fetal Lymphoid Organ Immune Responses to Transient and Persistent Infection with Bovine Viral Diarrhea Virus." Viruses 12, no. 8 (July 28, 2020): 816. http://dx.doi.org/10.3390/v12080816.
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Bovine Viral Diarrhea Virus (BVDV) fetal infections occur in two forms; persistent infection (PI) or transient infection (TI), depending on what stage of gestation the fetus is infected. Examination of lymphoid organs from both PI and TI fetuses reveals drastically different fetal responses, dependent upon the developmental stage of the fetal immune system. Total RNA was extracted from the thymuses and spleens of uninfected control, PI, and TI fetuses collected on day 190 of gestation to test the hypothesis that BVDV infection impairs the innate and adaptive immune response in the fetal thymus and spleen of both infection types. Transcripts of genes representing the innate immune response and adaptive immune response genes were assayed by Reverse Transcription quatitative PCR (RT-qPCR) (2−ΔΔCq; fold change). Genes of the innate immune response, interferon (IFN) inducible genes, antigen presentation to lymphocytes, and activation of B cells were downregulated in day 190 fetal PI thymuses compared to controls. In contrast, innate immune response genes were upregulated in TI fetal thymuses compared to controls and tended to be upregulated in TI fetal spleens. Genes associated with the innate immune system were not different in PI fetal spleens; however, adaptive immune system genes were downregulated, indicating that PI fetal BVDV infection has profound inhibitory effects on the expression of genes involved in the innate and adaptive immune response. The downregulation of these genes in lymphocytes and antigen-presenting cells in the developing thymus and spleen may explain the incomplete clearance of BVDV and the persistence of the virus in PI animals while the upregulation of the TI innate immune response indicates a more mature immune system, able to clear the virus.
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Marchalonis, John J., Peter J. Morris, and Alan W. Harris. "SPECULATIONS ON THE FUNCTION OF IMMUNE RESPONSE GENES." International Journal of Immunogenetics 1, no. 1 (April 2, 2007): 63–67. http://dx.doi.org/10.1111/j.1744-313x.1974.tb00292.x.
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Blumenthal, M., B. Johnson, D. Marcus, C. Alper, N. Mendell, H. Thode, and E. Yunis. "558 Immune response genes of ragweed sensitive individuals." Journal of Allergy and Clinical Immunology 81, no. 1 (January 1988): 307. http://dx.doi.org/10.1016/0091-6749(88)90792-0.
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Damulewicz, Milena, Michał Świątek, Agnieszka Łoboda, Józef Dulak, Bernadetta Bilska, Ryszard Przewłocki, and Elżbieta Pyza. "Daily Regulation of Phototransduction, Circadian Clock, DNA Repair, and Immune Gene Expression by Heme Oxygenase in the Retina of Drosophila." Genes 10, no. 1 (December 21, 2018): 6. http://dx.doi.org/10.3390/genes10010006.
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The daily expression of genes and the changes in gene expression after silencing the heme oxygenase (ho) gene were examined in the retina of Drosophila using microarray and SybrGreen qPCR (quantitative polymerase chain reaction) methods. The HO decrease in the morning upregulated 83 genes and downregulated 57 genes. At night, 80 genes were upregulated and 22 were downregulated. The top 20 genes downregulated after ho silencing in the morning modulate phototransduction, immune responses, autophagy, phagocytosis, apoptosis, the carbon monoxide (CO) response, the oxidative stress/UV response, and translation. In turn, the genes that upregulated at night were involved in translation—the response to oxidative stress, DNA damage, and phototransduction. Among the top 20 genes downregulated at night were genes involved in phototransduction, immune responses, and autophagy. For some genes, a low level of HO had an opposite effect in the morning compared to those at night. Silencing ho also changed the expression of circadian clock genes, while the HO decrease during the night enhanced the expression of immune system genes. The results showed that the cyclic expression of HO is important for controlling several processes in the retina, including neuroprotection and those involved in the innate immune system.
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Hsu, S. D., C. K. Anders, C. R. Acharya, Y. Zhang, Y. Wang, J. A. Foekens, K. L. Blackwell, C. G. Drake, M. A. Morse, and P. G. Febbo. "Immune signatures hold prognostic import across solids tumors." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 21041. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21041.
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21041 Background: The host immune response can impact cancer growth, prognosis, and response to therapy. In colorectal cancer, the presence of cells involved with T-cell mediated adaptive immunity better predicts of survival than the current staging method. Immune signatures based on host response to cancer have the potential to predict prognosis and facilitate target specific therapy. Methods: We used the gene expression data associated with immune host response to colorectal cancer (Galon et al., Science 2006) to perform hierarchical clustering of solid tumors for which the clinical annotation were available. Specifically, prostate (n=79), breast (n=132), lung (n=37), and lymphoma (n=127) samples were clustered based upon expression of genes associated with host immune responses (Th1 mediated adaptive immunity (Th1), inflammation, and immune suppression (IS)). Kaplan-Meier survival analysis was then used to determine if major sample clusters had significantly different disease free survival. Results: Clusters with differential prognosis (disease free survival) were consistently seen across all tumors. Among adenocarcinomas, and similar to previously published colorectal data, the Th1 genes were consistently associated with better prognosis. Specifically, in breast cancer patients, increased expression of the Th1 genes was protective, but only in patients under 45 years of age (HR=0.42; p=0.05). In prostate cancer, patients with increased expression of the Th1 genes and inflammation genes had better prognosis when compared to those without the Th1 genes (HR=0.36; p=0.03) or inflammation genes (HR=0.37; p=0.03). Lung cancer patients expressing the Th1 genes and IS genes appear to have improved survival when compared to those without the IS genes (HR=0.33; p=0.08). In contrast, Th1 genes were associated with poorer prognosis in lymphoma patients. Patients with decreased Th1 genes and increased expression of inflammation genes had better prognosis than those expressing the Th1 genes (HR=0.43; p=0.013) or IS genes (HR= 0.35; p=0.002) only. Conclusions: Signatures of the host immune response to solid tumors hold prognostic significance. Future work will determine if immune signatures can be predictive of response to therapy and help guide management. No significant financial relationships to disclose.
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Wu, Louisa P., Kwang-Min Choe, Yiran Lu, and Kathryn V. Anderson. "Drosophila Immunity: Genes on the Third Chromosome Required for the Response to Bacterial Infection." Genetics 159, no. 1 (September 1, 2001): 189–99. http://dx.doi.org/10.1093/genetics/159.1.189.
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Abstract We have screened the third chromosome of Drosophila melanogaster for mutations that prevent the normal immune response. We identified mutant lines on the basis of their failure to induce transcription of an antibacterial peptide gene in response to infection or their failure to form melanized clots at the site of wounding. These mutations define 14 genes [immune response deficient (ird) genes] that have distinct roles in the immune response. We have identified the molecular basis of several ird phenotypes. Two genes, scribble and kurtz/modulo, affect the cellular organization of the fat body, the tissue responsible for antimicrobial peptide production. Two ird genes encode components of the signaling pathways that mediate responses to bacterial infection, a Drosophila gene encoding a homolog of IκB kinase (DmIkkβ) and Relish, a Rel-family transcription factor. These genetic studies should provide a basis for a comprehensive understanding of the genetic control of immune responses in Drosophila.
Dissertations / Theses on the topic "Immune response genes"
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Aldred, Patricia M. R. "Variation in human immune response genes." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415720.
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Lorenzi, Roberto. "Studies on gene conversion as a mutational mechanism in the evolution of major histocompatibility complex genes." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336766.
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Milner, Caroline M. "Characterisation of novel genes in the human major histocompatibility complex : the HSP70 & G9a genes." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302867.
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Ghaffari, Emma Louise Marie. "Early growth response genes -2 and -3 are essential for optimal immune responses." Thesis, Brunel University, 2013. http://bura.brunel.ac.uk/handle/2438/8134.
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Early Growth Response Genes (EGR) is a family of four transcription factors containing a unique zinc finger domain. EGR-2 and EGR-3 are important for hindbrain development and myelination. These transcription factors are also necessary for lymphocyte function however, the mechanisms are still unclear. Previous findings have shown that EGR-2cKO mice develop lupus-like autoimmune disease with high levels of pro-inflammatory cytokines despite showing normal T and B cell proliferation after mitogenic stimulation. Therefore we established the CD2-EGR-2-/-EGR-3-/- mouse model to explore the phenotype, susceptibility to autoimmune disease and relevant lymphocyte function. We discovered that CD2-EGR-2-/-EGR-3-/- mice developed severe systemic autoimmune disease and expressed high levels of inflammatory cytokines. More importantly we discovered a novel finding that CD2-EGR-2-/-EGR-3-/- T and B cells had impaired cell proliferation after mitogenic stimulation. Further investigations revealed that the molecular mechanism defected in the T cell receptor signalling pathway is due to a dysfunction in Activator Protein-1 (AP-1). AP-1 is a heterodimeric protein composed of AP-1 family members including Jun, Atf and Fos. Our data shows that EGR-2 and EGR-3 directly bind with the Atf family member Batf, which prevents Batf’s inhibitory function on AP-1 activation. This research demonstrates that EGR-2 and EGR-3 intrinsically regulate chronic inflammation and also positively regulate antigen receptor activation. In conclusion EGR-2 and EGR-3 are essential for providing optimal immune responses, whilst limiting inflammatory immunopathology. We propose that this new model could be used for studying autoimmune disease.
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Kendall, Elaine. "Molecular characterisation of the human major histocompatibility complex." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333402.
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O'Neill, Ann Marie Ewald Sandra J. "Polymorphism in chicken immune response genes and resistance to disease." Auburn, Ala., 2007. http://repo.lib.auburn.edu/2007%20Fall%20Dissertations/O'Neill_Ann_48.pdf.
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Daniels, Garry D. "Cloning and characterisation of cytokine and cytokine receptor genes in rainbow trout, Oncorhynchus mykiss." Thesis, University of Aberdeen, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265893.
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Convincing molecular evidence for the existence of both cytokines and their receptors in teleost fish is presented. TGF-β is present in O. mykiss encoding a 112 amino acid mature peptide. An integrin binding site (RGD) and a characteristic tetrabasic cleavage site (RKKR) are present, as is the TGF-β superfamily motif. The mature peptide has 9 conserved cysteine residues (8 of which occur in pairs) as well as two additional conserved TGF-β superfamily residues (Pro36 and Gly46). TGF-β exhibits a wide range tissue distribution including head-kidney macrophages, PBL, brain, gill and spleen tissue, and is encoded by a 2.5Kb mRNA. The trout TGF-β gene is spread over 7 exons, with an additional intron in exon 7 when compared to mammalian and avian models. Isolation of a partial sequence also reveals the presence of TGF-β in a cyprinid species. Phylogenetic analysis suggests trout TGF-β to cluster with mammalian TGF-β1 isoforms, and the avian (TGF-β4) and amphibian (TGF-β5) homologs. Neither TNF-α or TNF receptors were detected in O. mykiss at either the cellular or molecular level. The use of degenerate primers in PCR lead to the isolation of a partial sequence for O. mykiss MHC class I. A full length CXC-R gene of 1.6Kb isolated from O. mykiss displays approximately 65% identity to mammalian CXC-R4 receptors, exhibits the seven-transmembrane domain structure of the G-protein coupled receptors and a tissue-specific distribution. Characteristic superfamily motifs and a putative glycosylation site are present in the sequence. Along with the major features of the adaptive immune response such as the major histocompatibility complex (MHC), T-cell receptor (TCR) and immunoglobulin (Ig), cytokines are now shown to be present at the level of teleost fish.
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Emonts, M. "Polymorphisms in immune response genes in infectious diseases and autoimmune diseases." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/14316.
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Modesto, P. "EXPRESSION PROFILE OF IMMUNE RESPONSE GENES IN GOATS WITH EXPERIMENTALLY INDUCED STAPHYLOCOCCUS AUREUS MASTITIS." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/169565.
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Counteracting infectious diseases of farm animals are an everlasting challenge in food production from livestock and preserving the health of farm animals is highly relevant to maintaining high standards of food quality. Clinical mastitis (CM) is the primary health reason for involuntary culling in dairy small ruminants and causes additional economic losses from costs of veterinary treatments. Complementary strategies are needed, since the classical prophylactic measures sometimes appear too demanding to breeders in terms of time and care, and efficient vaccination against the main pathogens is still lacking. There is evidence that Somatic Cell Count (SCC)-based selection should efficiently reduce CM incidence and currently selection strategies in cows and sheeps are based on a linear decrease of milk SCC. The effects and efficacy of SCC selection in goats are still unknown. A better understanding of the defense mechanisms affected and modified by SCC-based selection would be helpful to predict the indirect response for CM, pathogen-specific infections, and resistance to other diseases in the long term. Knowledge of these basic mechanisms will help to the design new and optimized strategies to prevent infections and, at the same time, significantly aid the improvement of food safety for the consumer. Microarray technology enables the examination of complex interactions between the host and bacterial pathogens. In dairy ruminants transcriptome profiling has enabled the identification of genes, pathways and regulatory networks activated in mammary tissues during experimental infection by various pathogens, including E. coli, S. aureus and S. uberis. Information in goats are still low and many host-pathogen interaction mechanisms have to be explained. In our study the bovine CustomArray 90K was used to evaluate the gene expression in milk somatic cells (MSCs) and blood of goats infected by S. aureus.The objectives of the present study were: (i) to identify the network of genes that becomes activated in caprine blood and MSCs in early response upon a S. aureus challenge in order to better understand the local and sistemic response and (ii) to search any difference in this immune response by using two animal groups belonging to a caprine reference family established based on founders with adverse SCC breeding values, (iii) to develop a set of internal reference genes useful to normalize RT-qPCR data in studies of gene expression in caprine MSCs. A total of 300 genes were found to be differentially expressed between 0 h and 24 h post infection and 128 genes between 0 h and 30 h post infection, with a p value < 0.01 and log2 fold change > 1.5. Among these, the majority were up-regulated. In leukocytes a total of 8 genes were up-regulated between 0h and 30h post infection with a p value < 0.01 and log2 fold change > 1.5 and 1 was down-regulated during IMI. The top up-regulated genes (5.65 to 3.16 fold change) plays an important role (i) in immune and inflammatory response (NFKB1, TNFAIP6, BASP1, IRF1, PLEK, BATF3); (ii) in the regulation of innate resistance to pathogens (PTX3); (iii) in the regulation of cell metabolism (CYTH4, SLC2A6, ARG2). The top down-regulated genes (-1.50 to –2.46 fold) included genes involved in lipid metabolism (ABCG2, FASN), chemokine, cytokine and intracellular signaling (SPPI), cytoskeleton and extracellular matrix (KRT19). No significant differences were found in the levels of the expression gene between the two group of animals. Results provided novel information into the early stage of S. aureus infection in goats. Moreover, this study provides a validated panel of optimal internal references genes which may be useful for the identification of genes differentially expressed by RT-qPCR in caprine MSCs. According to our evaluation, we recommend using G6PD and YWHAZ as reference genes to normalize gene expression data in caprine MSCs.
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MAGRO, GIADA. "BOVINE STAPHYLOCOCCUS AUREUS MASTITIS: FROM THE MAMMARY IMMUNE RESPONSE TO THE BACTERIA VIRULENCE GENES." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/548380.
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Staphylococcus aureus (S. aureus) is one of the most important bacteria in veterinary medicine. In dairy herds, it is a contagious bacterium responsible mainly for subclinical mastitis in cattle, which frequently gives rise to persistent and chronic infection. Mastitis cause considerable economic losses due to i) decreased milk production, (ii) reduced milk quality, and (iii) treatment costs. Mastitis is also a public health problem. Indeed, the strains isolated from infected glands could produce enterotoxins. Three factors interact in mastitis: the host, the pathogen and the environment. This thesis focuses on two main aspects: the host immune response and the virulence factor of S. aureus.
The first chapter of the thesis focused on the development of a new mammary gland model to study the innate immune response bacterial infection. The mammary gland is a complex organ, and the immune response is a consequence of the different cell population interactions. Continuous or primary epithelial cell lines have been extensively used to study the mammary gland immune response, but they are composed of a single cell population.
Previous studies explored the tissues of lactating cows, unconsidering the possibility of an already triggered immune response. To investigate the innate immune response of the bovine mammary gland, we used an explant of healthy heifer gland. This model allowed us to: i) exclude previous exposure of the udder to microorganisms, which might have damaged the cells and/or triggered an immune response, and ii) consider the interaction of the challenging microorganism with the tissue cell populations.
Our aim was to test whether this innovative model might be a valid model to investigate the innate immune response to infection. The study was carried out on 2 mm3-sections of heifer udders, in 2 consecutive trials, using LPS or LTA in the first trial and two different concentrations of S. aureus in the second. Treated and untreated sections were collected after 1h, 3h and 6h incubation; in the first trial, a final time-point at 18h was considered. The mRNA expression of TNFα, IL-1β, IL-6, IL-8 and LAP was analyzed by quantitative real-time PCR. Histological examination showed well-preserved morphology of the tissue, and apoptosis only showed a slight, not significant increase throughout the experiment. IL-1β and IL-6 were significantly up-regulated, in response to LPS or S. aureus, while TNF-α and IL-8 significantly increased only under LPS treatment. LAP expression showed a significant late increase when stimulated by LPS. The immunochemical staining of the sections demonstrated a higher number of T lymphocytes within the alveolar epithelium, in comparison with interstitial localization. Since the explants belonged to pubertal non-pregnant heifers, T cells may be regarded as resident cells, suggesting their participation in the regulation of mammary homeostasis. Therefore, applying our model would give new insights in the investigation of udder pathophysiology.
The second chapter of the thesis focused on S. aureus in bovine intrammary infections. Previous literature on the S. aureus-intrammamary suggested that infection might be related to a combination of S. aureus virulence factors beyond host factors. The present study considered 169 isolates from different Italian dairy herds that were classified into four groups based on the prevalence of S. aureus infection at the first testing: low prevalence (< 5 %; LP), medium–low (5.1 - 24 %; MLP), medium–high (24.1 - 40 %; MHP) and high (> 40 %; HP). We aimed to correlate the presence of virulence genes with the herd prevalence of intramammary infections in order to develop new strategies for the control of S. aureus mastitis. Microarray data were statistically evaluated using binary logistic regression and correspondence analysis to screen the risk factors and the relationship between prevalence group and gene. The analysis showed: (1) 24 genes at significant risk of being detected in all the herds with infection prevalence >5%, including genes belonging to microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), immune evasion and serine proteases; and (2) a significant correlation coefficient between the genes interacting with the host immune response and HP isolates against LP ones. These results support the hypothesis that virulence factors, in addition to cow management, could be related to strain contagiousness, offering new insights into vaccine development.
Books on the topic "Immune response genes"
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Mak, Tak W. Handbook of immune response genes. New York: Plenum Press, 1998.
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Marc, Feldmann, and McMichael Andrew J, eds. Regulation of immune gene expression. Clifton, N.J: Humana Press, 1986.
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J, Kay, ed. Genes and proteins in immunity. London: Biochemical Society, 1986.
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B, Schook Lawrence, Tew John G, and International RES Symposium (1987 : Richmond, Va.), eds. Antigen presenting cells: Diversity, differentiation, and regulation : proceedings of a symposium held in Richmond, Virginia, March 26-29, 1987. New York: Liss, 1988.
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Ottenhoff, Thomas Henricus Maria. HLA class II immune response genes in leprosy: Studies on the recognition of Mycobacterium leprae antigens and class II molecules by cloned human T cells. [s.l.]: [s.n.], 1986.
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Derek, Wakelin, and Blackwell J. M, eds. Genetics of resistance to bacterial and parasitic infection. London: Taylor & Francis, 1988.
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1943-, Watson James D., and Marbrook John, eds. Recognition and regulation in cell-mediated immunity. New York, N.Y: M. Dekker, 1985.
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Mak, Tak W., and John J. L. Simard. Handbook of Immune Response Genes. Springer, 2013.
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Feldmann, Marc, and Andrew McMichael. Regulation of Immune Gene Expression. Humana Press, 2012.
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Feldmann, Marc, and Andrew McMichael. Regulation of Immune Gene Expression. Humana Press, 2012.
Find full textBook chapters on the topic "Immune response genes"
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Winchester, Robert. "Human Immune Response Genes." In Immunopharmacology in Autoimmune Diseases and Transplantation, 3–14. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-1167-4_1.
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Nepom, Gerald T., and John A. Hansen. "Human Immune Response Genes." In Immunology of Rheumatic Diseases, 3–19. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2493-5_1.
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Bontrop, R. E. "MHC Genes, Immune Response, and Vaccines." In Molecular Biology and Evolution of Blood Group and MHC Antigens in Primates, 449–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59086-3_20.
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GÜnther, E. "Heat Shock Protein Genes and the Major Histocompatibility Complex." In Heat Shock Proteins and Immune Response, 57–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75875-1_3.
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Bell, J. I., and H. O. McDevitt. "Molecular Polymorphism of Human Immune-Response-Genes." In HLA Class II Antigens, 442–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70367-6_26.
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Greco, Raffaella, and Dominique Farge. "CART Cells and Other Cell Therapies (ie MSC, Tregs) in Autoimmune Diseases." In The EBMT Handbook, 837–48. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_93.
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AbstractAuto-immune diseases (AD) are heterogeneous conditions, characterized by polyclonal activation of the immune system with a defect of B or T lymphocyte selection and altered lymphocytic reactions to auto-antigens components (Burnet 1959a, b), although it is rare to identify a single antigenic epitope. The native immune system and its tissue environment play an important role to determine if exposure to a given antigen will induce an immune response or tolerance or anergy. The role of the genes coding for the major histocompatibility system molecules, but also of many other genes, is important in the regulation of the immune response, although this does not explain all the observed phenomena during loss of tolerance (Matzinger 1994; Rioux and Abbas 2005).
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Meignier, Bernard, and Bernard Roizman. "Genetic Engineering and Properties of Novel Herpes Simplex Viruses for Use as Potential Vaccines and as Vectors of Foreign Genes." In The Immune Response to Viral Infections, 187–92. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5712-4_17.
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Allan, Alison L., and Ann F. Chambers. "Genes and metastasis: experimental advances and clinical implications." In Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response, 33–58. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6729-7_4.
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Running, Katherine L. D., and Justin D. Faris. "Rapid Cloning of Disease Resistance Genes in Wheat." In Compendium of Plant Genomes, 187–212. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-38294-9_10.
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AbstractWheat is challenged by rapidly evolving pathogen populations, resulting in yield losses. Plants use innate immune systems involving the recognition of pathogen effectors and subsequent activation of defense responses to respond to pathogen infections. Understanding the genes, genetic networks, and mechanisms governing plant-pathogen interactions is key to the development of varieties with robust resistance whether through conventional breeding techniques coupled with marker selection, gene editing, or other novel strategies. With regards to plant-pathogen interactions, the most useful targets for crop improvement are the plant genes responsible for pathogen effector recognition, referred to as resistance (R) or susceptibility (S) genes, because they govern the plant’s defense response. Historically, the molecular identification of R/S genes in wheat has been extremely difficult due to the large and repetitive nature of the wheat genome. However, recent advances in gene cloning methods that exploit reduced representation sequencing methods to reduce genome complexity have greatly expedited R/S gene cloning in wheat. Such rapid cloning methods referred to as MutRenSeq, AgRenSeq, k-mer GWAS, and MutChromSeq allow the identification of candidate genes without the development and screening of high-resolution mapping populations, which is a highly laborious step often required in traditional positional cloning methods. These new cloning methods can now be coupled with a wide range of wheat genome assemblies, additional genomic resources such as TILLING populations, and advances in bioinformatics and data analysis, to revolutionize the gene cloning landscape for wheat. Today, 58 R/S genes have been identified with 42 of them having been identified in the past six years alone. Thus, wheat researchers now have the means to enhance global food security through the discovery of R/S genes, paving the way for rapid R gene deployment or S gene elimination, manipulation through gene editing, and understanding wheat-pathogen interactions at the molecular level to guard against crop losses due to pathogens.
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Nissar, Saniya, Aga Syed Sameer, and Mujeeb Zafar Banday. "Genetic Polymorphisms of Essential Immune Pathogenic Response Genes and Risk of Cervical Cancer." In Genetic Polymorphism and cancer susceptibility, 191–233. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6699-2_7.
Full textConference papers on the topic "Immune response genes"
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Zinovieva, S. V., Z. V. Udalova, and F. K. Khasanov. "EXPRESSION OF IMMUNE SYSTEM GENES IN TOMATO PLANTS INFECTED BY MELOIDOGYNE INCOGNITA." In THEORY AND PRACTICE OF PARASITIC DISEASE CONTROL. VNIIP – FSC VIEV, 2024. http://dx.doi.org/10.31016/978-5-6050437-8-2.2024.25.135-139.
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Data were presented from a study on expression of resistance gene Mi-1.2 of protective genes of the PR gene family (PR-2, PR-3) and genes of serine and cysteine proteinase (PIser PIcys) inhibitors in tissues of tomato plants of resistant and susceptible hybrids infected by gall nematodes and an assessment of their role in parasite resistance was given. Differences were detected in the expression of the studied genes at all stages of nematode development in the roots of resistant and susceptible plants. The studies showed that the infection of resistant plants caused an increase in the study gene transcripts as early as in the initial period of infection, which indicated the response time to nematode larvae penetration and the speed of adequate protective response. Changes in the defense response-related gene expression in infected susceptible plants were insignificant and appeared after the larvae penetrated the roots, which may be one of the reasons for disease progress. The increased expression of the studied genes that encode protective proteins in infected roots of resistant plants found at all parasite development stages indicates the importance of protective proteins in tomato plant resistance to gall nematode.
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Liu, Xiao-Ling. "DECIPHERING THE GENETIC LINKS BETWEEN PSYCHOLOGICAL STRESS, AUTOPHAGY, AND DERMATOLOGICAL HEALTH: INSIGHTS FROM BIOINFORMATICS, SINGLE-CELL ANALYSIS, AND MACHINE LEARNING IN PSORIASIS AND ANXIETY DISORDERS." In BioClina 2024 – International Conference on Biological & Clinical Studies, 21-22 June, Singapore. Global Research & Development Services, 2024. http://dx.doi.org/10.20319/icrlsh.2024.8687.
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The relationship between psychological stress, altered skin immunity, and autophagy-related genes (ATGs) is currently unclear. Psoriasis is a chronic skin inflammation of unclear etiology that is characterized by persistence and recurrence. Immune dysregulation and emotional disturbances are recognized as significant risk factors. Emerging clinical evidence suggests a possible connection between anxiety disorders, heightened immune system activation, and altered skin immunity, offering a fresh perspective on the initiation of psoriasis. The aim of this study was to explore the potential shared biological mechanisms underlying the comorbidity of psoriasis and anxiety disorders. Psoriasis and anxiety disorders data were obtained from the GEO database. A list of 3254 ATGs was obtained from the public database. Differentially expressed genes (DEGs) were obtained by taking the intersection of DEGs between psoriasis and anxiety disorder samples and the list of ATGs. Five machine learning algorithms used screening hub genes. The ROC curve was performed to evaluate diagnostic performance. Then, GSEA, immune infiltration analysis, and network analysis were carried out. The Seurat and Monocle algorithms were used to depict T-cell evolution. Cellchat was used to infer the signaling pathway between keratinocytes and immune cells. Four key hub genes were identified as diagnostic genes related to psoriasis autophagy. Enrichment analysis showed that these genes are indeed related to T cells, autophagy, and immune regulation, and have good diagnostic efficacy validated. Using single-cell RNA sequencing analysis, we expanded our understanding of key cellular participants, including inflammatory keratinocytes and their interactions with immune cells. We found that the CASP7 gene is involved in the T-cell development process, and correlated with γδ T cells, warranting further investigation. We found that anxiety disorders are related to increased autophagy regulation, immune dysregulation, and inflammatory response, and are reflected in the onset and exacerbation of skin inflammation. The hub gene is involved in the process of immune signaling and immune regulation. The CASP7 gene, which is related with the development and differentiation of T cells, deserves further study. Potential biomarkers between psoriasis and anxiety disorders were identified, which are expected to aid in the prediction of disease diagnosis and the development of personalized treatments.
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Uvarova, A. N., E. A. Tkachenko, K. V. Korneev, and D. V. Kuprash. "FUNCTIONAL ANALYSIS OF SNPS ASSOCIATED WITH SEVERE VIRAL RESPIRATORY DISEASES AND LOCATED IN THE REGULATORY REGIONS OF ANTIVIRAL IMMUNE RESPONSE GENES." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-378.
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We investigated the regulatory regions of the CD55, LGALS1, and IFNAR2 genes in cell models of human macrophages and B-cells and analyzed several SNPs located in the regulatory regions of these genes and associated with severe COVID-19 or flu. In the course of this work, we characterized the IFNAR2 gene enhancer and performed functional annotation of several SNPs in the CD55 and LGALS1 promoters.
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Muntyan, Victoria S., Alla S. Saksaganskaia, Alexey N. Muntyan, Mariia E. Vladimirova, and Marina L. Roumiantseva. "STRESS AND IMMUNITY OF NODULE BACTERIA SINORHIZOBIUM MELILOTI: LOCALIZATION, POLYMORPHISM AND PHYLOGENY OF GENETIC DETERMINANTS." In 22nd SGEM International Multidisciplinary Scientific GeoConference 2022. STEF92 Technology, 2022. http://dx.doi.org/10.5593/sgem2022/6.1/s25.15.
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Sinorhizobium meliloti are agriculturally valuable species of soil bacteria that form nitrogen-fixing symbiosis with alfalfa plants. Global climate changes lead to an increase of agricultural areas subjected to salinity. Current knowledge about about high-salt stress impact on soil saprophitic root nodulated microsymbionts of legumes is weakly studied and rhizobia gene pool responsible for salt tolerance are fragment and far from clear. An increase of bacteria nonspecific resistance (immune status) to unfavorable stress factors can occur through the induction of defense mechanisms like restrictionmodification systems and CRISPR/cas systems which are aimed to protect bacteria cells from bacteriophages widespread in soil microbiome. The aim of this research was to evaluate the role of the megaplasmid pSymA in the formation of ecological genome of S. meliloti, which is related to stress tolerance and to determine the location of elements of adaptive immune systems protecting root nodule bacteria against external foreign DNA. The analysis was done on 11 genes, products of which involved in response to ion stress and synthesis of osmoprotectors. It was found that 6 out of 11 genes were found in the genomes of all analyzed S. meliloti strains, while it was not a case for other 5 genes. It was found that, unlike chromosome, megaplasmid I of S. meliloti accumulated copies of 4 from 5 genes, except kdpA gene, which is represented by a single copy and localized on megaplasmid I in all so far studied strains. It was predicted that closest phylogenetic relatives of genes whose products are involved in response to ion stress as well in synthesis of osmoprotectors are homologous genes of closely related S. medicae species. The exception was for betI2, for which the closest phylogenetic relative was homologous gene of Klebsiella pneumonia, and another exception is kdpA gene introduced onto megaplasmid-I from actinobacteria. Regarding elements of immune systems it was revealed that nonsymbiotic plasmids of S. meliloti harbored incomplete elements of RMS-I, -II, and - III systems, while the 4 complete RMS-IV systems were detected on a single plasmid. It was found out that corresponding methylases had similarities with similar enzymes detected in nitrogen-fixing strains of Agrobacterium tumefaciens, Mezorhizobium sp., Bradyrhizobium sp. CRISPR sequences were not detected on megaplasmid-I, while they were on chromosome, megaplasmid-II and on cryptic plasmids. So, it was concluded that megaplasmid-I of S. meliloti are enriched in copies of genes related to osmotic stress tolerance, but it role in immune status of rhizobia is requested further elucidation.
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Buslaev, V. Yu, A. V. Torgunakova, Irina Milentyeva, Lyubov Dyshlyuk, and V. I. Minina. "POPYMORPHISM OF IMMUNE RESPONSE GENES AND LUNG CANCER RISK IN NON-SMOKING RESIDENTS OF KUZBASS." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-17.
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Lung cancer (LC) is leading oncological pathology, posing a serious threat for patient’s lives.
Accordingly to World Health Organization (WHO) 2,1 million of new cases and 1,8 of deaths are
annually registered. It was accumulated a lot of information about significant influence of smoking on
increased risk of LC development. 80-90% of patients with LC are namely smokers. However at present
time it was registered increased level of mortality from this pathology among non-smoking patients [1].
LC formation in non-smoking individuals can occur due to environmental pollution by industrial and
household cancerogens and also because of molecular and genetical and cytogenetical dissimilarities.
Since LC development can be associated with anomalous immunological response, immune genes can
be considered as potential biological markers [2].
Objective: To assess the influence of polymorphic variants of innate immunity genes on LC
development in non-smoking patients.
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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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Chumacheva, Yu V., and D. S. Stashkevich. "COMBINATIONS OF SNPS TNFRSF11B AND TNFA GENOTYPES IN PATIENTS WITH RHEUMATOID ARTHRITIS OF THE BASHKIR POPULATION IN CHELYABINSK REGION." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-392.
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Cytokine genes influence the nature of the immune response in rheumatoid arthritis (RA) through the level of production of encoded proteins, which makes the functional polymorphism of cytokine genes particularly interesting for research in RA. In our study, we evaluated combinations of frequencies of combinations genotype of polymorphisms of TNFRSF11B genes at point G1181C and TNFA at points G-308A, G-238A in population of Bashkir RA patients and a control group to identify possible associations.
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Han, Sohee, Qing Lan, Ae Kyung Park, Kyoung-Mu Lee, Sue K. Park, Hyo Seop Ahn, Hee Young Shin, et al. "Abstract 925: Common variants in genes related to immune response and childhood leukemia risk." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-925.
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Mbofung, Rina M., Jodi A. McKenzie, Shruti Malu, Chengwen Liu, Leila Williams, Weiyi Peng, Zhe Wang, et al. "Abstract 4360: Inhibition of HSP90 enhances T cell-mediated antitumor immune responses through expression of interferon-alpha response Genes." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4360.
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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.
Reports on the topic "Immune response 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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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.
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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, July 2004. http://dx.doi.org/10.32747/2004.7587236.bard.
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Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show 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 (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.
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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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David, Lior, Yaniv Palti, Moshe Kotler, Gideon Hulata, and Eric M. Hallerman. Genetic Basis of Cyprinid Herpes Virus-3 Resistance in Common Carp. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7592645.bard.
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The goal of this project was to provide scientific and technical basis for initiating the development of breeding protocols using marker assisted selection for viral disease resistance in common carp. The specific objectives were: 1) Establishing families and characterizing the phenotypic and genetic variation of viral resistance; 2) Measuring the dynamics of immune response and developing a method to measure the long term immune memory; 3) Developing markers and generating a new genetic linkage map, which will enable initial QTL mapping; and, 4) Identifying genetic linkage of markers and candidate genes (like MHC and TLRs) with resistance to CyHV-3. The common carp is an important farmed freshwater fish species in the world. Edible carp is second only to tilapia in Israeli aquaculture production and ornamental carp (koi) is an important product in both the US and Israel. Carp industries worldwide have recently suffered enormous economic damage due to a viral disease caused by Cyprinid herpes virus 3 (CyHV-3). Aside from preventative measures, a sustainable solution to this problem will be to establish a genetic improvement program of the resistance of fish to the pathogen. The aims of the project was to take the necessary first steps towards that. The differences in survival rates after infection with CyHV-3 virus among 20 families from six types of crosses between three carp lines (two commercial lines and one wild-type carp) revealed that the wild-type carp and its crosses had a much-improved survival over the crosses of the commercial lines themselves. These crosses set the starting point for breeding of commercial strains with improved resistance. Resistant fish had lower antibody titer against the virus suggesting that resistance might depend more on the innate immunity. A set of 500 microsateliite markers was developed and the markers are currently being used for generating a genetic linkage map for carp and for identifying disease resistance QTL. Fourteen candidate immune genes, some of which were duplicated, were cloned from the carp and SNP markers were identified in them. The expression of these genes varied between tissues and suggested functional divergence of some duplicated genes. Initial association between CyHV-3 resistance and one of the genes was found when SNP alleles in these genes were tested for their segregation between susceptible and resistant progeny. The results of this project have implications to the development of viral resistant commercial carp strains and effective immunization against this aggressive disease. The genetic and immunological knowledge accumulated in this project will not only promote carp and koi production but will also contribute to a broader understanding of fish immunogenetics.
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McElwain, Terry F., Eugene Pipano, Guy H. Palmer, Varda Shkap, Stephn A. Hines, and Wendy C. Brown. Protection of Cattle against Babesiosis: Immunization against Babesia bovis with an Optimized RAP-1/Apical Complex Construct. United States Department of Agriculture, September 1999. http://dx.doi.org/10.32747/1999.7573063.bard.
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Previous research and current efforts at control of babesiosis fall short of meeting the needs of countries where the disease is endemic, such as Israel, as well as the needs of exporting countries and countries bordering on endemic areas, such as the U.S. Our long-term goal is to develop improved methods of immunization against bovine babesiosis based on an understanding of the molecular mechanisms of immune protection and parasite targets of a protective immune response. In our previous BARD project, we established the basis for focusing on rhoptry antigens as components of a subunit vaccine against bovine babesiosis, and for additional research to better characterize rhoptry associated protein-1 (RAP-1) as a target of protective immunity. In this continuation BARD project, our objectives were to [1] optimize the immune response against RAP-1, and [2] identify additional rhoptry candidate vaccine antigens. The entire locus encoding B. bovis RAP-1 was sequenced, and the rap-1 open reading frame compared among several strains. Unlike B. bigemina, in which multiple gene copies with variant domains encode RAP-1, the B. bovis RAP-1 locus contains only two identical genes which are conserved among strains. Through testing of multiple truncated constructs of rRAP-1, one or more immunodominant T cell epitopes were mapped to the amino terminal half of RAP-1. At least one linear and one conformational B cell epitope have been demonstrated in the same amino terminal construct, which in B. bigemina RAP-1 also contains an epitope recognized by neutralizing antibody. The amine terminal half of the molecule represents the most highly conserved part of the gene family and contains motifs conserved broadly among the apicomplexa. In contrast, the carboxy terminal half of B. bovis RAP-1 is less well conserved and contains multiple repeats encoding a linear B cell epitope potentially capable of inducing an ineffective, T cell independent, type 2 immune response. Therefore, we are testing an amino terminal fragment of RAP-1 (RAP-1N) in an immunization trial in cattle. Cattle have beer immunized with RAP-1N or control antigen, and IL-12 with Ribi adjuvant. Evaluation of the immune response is ongoing, and challenge with virulent B. bovis will occur in the near future. While no new rhoptry antigens were identified, our studies did identify and characterize a new spherical body antigen (SBP3), and several heat shock proteins (HSP's). The SBP3 and HSP21 antigens stimulate T cells from immune cattle and are considered new vaccine candidates worthy of further testing. Overall, we conclude that a single RAP-1 vaccine construct representing the conserved amino terminal region of the molecule should be sufficient for immunization against all strains of B. bovis. While results of the ongoing immunization trial will direct our next research steps, results at this time are consistent with our long term goal of designing a subunit vaccine which contains only the epitopes relevant to induction of protective immunity. Parallel studies are defining the mechanisms of protective immunity. Apicomplexan protozoa, including babesiosis and malaria, cause persistent diseases for which control is inadequate. The apical organelles are defining features of these complex protozoa, and have been conserved through the evolutionary process, Past and current BARD projects on babesiosis have established the validity and potential of exploiting these conserved organelles in developing improved control methods applicable to all apicomplexan diseases.
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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.
Full textAbstract:
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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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.
Full textAbstract:
In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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Sessa, Guido, and Gregory B. Martin. molecular link from PAMP perception to a MAPK cascade associated with tomato disease resistance. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597918.bard.
Full textAbstract:
The research problem: The detection of pathogen-associated molecular patterns (PAMPs) by plant pattern recognition receptors (PRRs) is a key mechanism by which plants activate an effective immune response against pathogen attack. MAPK cascades are important signaling components downstream of PRRs that transduce the PAMP signal to activate various defense responses. Preliminary experiments suggested that the receptor-like cytoplasmickinase (RLCK) Mai5 plays a positive role in pattern-triggered immunity (PTI) and interacts with the MAPKKK M3Kε. We thus hypothesized that Mai5, as other RLCKs, functions as a component PRR complexes and acts as a molecular link between PAMP perception and activation of MAPK cascades. Original goals: The central goal of this research was to investigate the molecular mechanisms by which Mai5 and M3Kε regulate plant immunity. Specific objectives were to: 1. Determine the spectrum of PAMPs whose perception is transmitted by M3Kε; 2. Identify plant proteins that act downstream of M3Kε to mediate PTI; 3. Investigate how and where Mai5 interacts with M3Kε in the plant cell; 4. Examine the mechanism by which Mai5 contributes to PTI. Changes in research directions: We did not find convincing evidence for the involvement of M3Kε in PTI signaling and substituted objectives 1 and 3 with research activities aimed at the analysis of transcriptomic profiles of tomato plants during the onset of plant immunity, isolation of the novel tomato PRR FLS3, and investigation of the involvement of the RLCKBSKs in PTI. Main achievements during this research program are in the following major areas: 1. Functional characterization of Mai5. The function of Mai5 in PTI signaling was demonstrated by testing the effect of silencing the Mai5 gene by virus-induced gene silencing (VIGS) experiments and in cell death assays. Domains of Mai5 that interact with MAPKKKs and subcellular localization of Mai5 were analyzed in detail. 2. Analysis of transcriptional profiles during the tomato immune responses to Pseudomonas syringae (Pombo et al., 2014). We identified tomato genes whose expression is induced specifically in PTI or in effector-triggered immunity (ETI). Thirty ETI-specific genes were examined by VIGS for their involvement in immunity and the MAPKKK EPK1, was found to be required for ETI. 3. Dissection of MAP kinase cascades downstream of M3Kε (Oh et al., 2013; Teper et al., 2015). We identified genes that encode positive (SGT and EDS1) and negative (WRKY1 and WRKY2) regulators of the ETI-associated cell death mediated by M3Kε. In addition, the MKK2 MAPKK, which acts downstream of M3Kε, was found to interact with the MPK3 MAPK and specific MPK3 amino acids involved interaction were identified and found to be required for induction of cell death. We also identified 5 type III effectors of the bacterial pathogen Xanthomonaseuvesicatoria that inhibited cell death induced by components of ETI-associated MAP kinase cascades. 4. Isolation of the tomato PRR FLS3 (Hind et al., submitted). FLS3, a novel PRR of the LRR-RLK family that specifically recognizes the flagellinepitope flgII-28 was isolated. FLS3 was shown to bind flgII-28, to require kinase activity for function, to act in concert with BAK1, and to enhance disease resistance to Pseudomonas syringae. 5. Functional analysis of RLCKs of the brassinosteroid signaling kinase (BSK) family.Arabidopsis and tomato BSKs were found to interact with PRRs. In addition, certain ArabidospsisBSK mutants were found to be impaired in PAMP-induced resistance to Pseudomonas syringae. Scientific and agricultural significance: Our research activities discovered and characterized new molecular components of signaling pathways mediating recognition of invading pathogens and activation of immune responses against them. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease.
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Chejanovsky, Nor, Diana Cox-Foster, Victoria Soroker, and Ron Ophir. Honeybee modulation of infection with the Israeli acute paralysis virus, in asymptomatic, acutely infected and CCD colonies. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7594392.bard.
Full textAbstract:
Honey bee (Apis mellifera) colony losses pose a severe risk to the food chain. The IAPV (Israeli acute paralysis virus) was correlated with CCD, a particular case of colony collapse. Honey bees severely infected with IAPV show shivering wings that progress to paralysis and subsequent death. Bee viruses, including IAPV, are widely present in honey bee colonies but often there are no pathological symptoms. Infestation of the beehive with Varroa mites or exposure to stress factors leads to significant increase in viral titers and fatal infections. We hypothesized that the honey bee is regulating/controlling IAPV and viral infections in asymptomatic infections and this control is broken through "stress" leading to acute infections and/or CCD. Our aims were: 1. To discover genetic changes in IAPV that may affect tissue tropism in the host, and/or virus infectivity and pathogenicity. 2. To elucidate mechanisms used by the host to regulate/ manage the IAPV-infection in vivo and in vitro. To achieve the above objectives we first studied stress-induced virus activation. Our data indicated that some pesticides, including myclobutanil, chlorothalonil and fluvalinate, result in amplified viral titers when bees are exposed at sub lethal levels by a single feeding. Analysis of the level of immune-related bee genes indicated that CCD-colonies exhibit altered and weaker immune responses than healthy colonies. Given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies were able to elicit this particular antiviral response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed high frequency of small interfering RNAs (siRNA) perfectly matching IAPV, Kashmir bee virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi pattern of targeting the viral genome .Our findings were further supported by analysis of samples from colonies experimentally infected with IAPV. Following for the first time the dynamics of IAPV infection in a group of CCD colonies that we rescued from collapse, we found that IAPV conserves its potential to act as one lethal, infectious factor and that its continuous replication in CCD colonies deeply affects their health and survival. Ours is the first report on the dominant role of IAPV in CCD-colonies outside from the US under natural conditions. We concluded that CCD-colonies do exhibit a regular siRNA response that is specific against predominant viruses associated with colony losses and other immune pathways may account for their weak immune response towards virus infection. Our findings: 1. Reveal that preventive measures should be taken by the beekeepers to avoid insecticide-based stress induction of viral infections as well as to manage CCD colonies as a source of highly infectious viruses such as IAPV. 2. Contribute to identify honey bee mechanisms involved in managing viral infections.