Academic literature on the topic 'Immune-related gene'
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Journal articles on the topic "Immune-related gene"
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Marta, M., P. Stridh, K. Becanovic, A. Gillett, J. Öckinger, J. C. Lorentzen, M. Jagodic, and T. Olsson. "Multiple loci comprising immune-related genes regulate experimental neuroinflammation." Genes & Immunity 11, no. 1 (August 13, 2009): 21–36. http://dx.doi.org/10.1038/gene.2009.62.
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Bottini, Fulvia Gloria, Neri A, Saccucci P, Manca Bitti M L, Rapini N, Magrini A, and Bottini E. "IMMUNE RELATED DISEASES AND THEIR RELATIONSHIP WITH THE GENETIC VARIABILITY WITHIN THE ADENOSINE DEAMINASE GENE." Journal of Advances In Allergy & Immunologic Diseases 3, no. 1 (2018): 1–8. http://dx.doi.org/10.25177/jaaid.3.1.1.
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Singh, Dhirendra P., Prathyusha Bagam, Malaya K. Sahoo, and Sanjay Batra. "Immune-related gene polymorphisms in pulmonary diseases." Toxicology 383 (May 2017): 24–39. http://dx.doi.org/10.1016/j.tox.2017.03.020.
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Hamidi, Yeganeh, Elaheh Aliasgari, Paria Basimi, Mansour Sajadipour, and Kazem Baesi. "Immune-Related Gene Profile in HIV-Infected Patients with Discordant Immune Response." Iranian Biomedical Journal 26, no. 6 (October 1, 2022): 485–91. http://dx.doi.org/10.52547/ibj.3750.
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Tziastoudi, Maria, Christos Cholevas, Ioannis Stefanidis, and Theoharis C. Theoharides. "Immune-Related Gene Polymorphisms and Pharmacogenetic Studies in Nephrology." Clinical Therapeutics 43, no. 12 (December 2021): 2148–53. http://dx.doi.org/10.1016/j.clinthera.2021.09.020.
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UMEDA, YUKIO. "Inhibition of Immune Responses by Calcitonin Gene-Related Peptide." Annals of the New York Academy of Sciences 657, no. 1 Calcitonin Ge (June 1992): 552–54. http://dx.doi.org/10.1111/j.1749-6632.1992.tb22832.x.
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Wang, Huiling, Shuo You, Meng Fang, and Qian Fang. "Recognition of Immune Microenvironment Landscape and Immune-Related Prognostic Genes in Breast Cancer." BioMed Research International 2020 (November 15, 2020): 1–16. http://dx.doi.org/10.1155/2020/3909416.
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Background. Breast cancer (BC) is the most common malignant tumor in women. The immunophenotype of tumor microenvironment (TME) has shown great therapeutic potential in tumor. Method. The transcriptome was obtained from TCGA and GEO data. Immune infiltration was analyzed by single-sample gene set enrichment (ssGSEA). The immune feature was constructed by Cox regression analysis. In addition, the coexpression of differential expression genes (DEGs) was identified. Through enrichment analysis, the function and pathway of module genes were identified. The somatic mutations related to immune characteristics were analyzed by Maftools. By using the consistency clustering algorithm, the molecular subtypes were constructed, and the overall survival time (OS) was predicted. Results. Immune landscape can be divided into low immune infiltration and high immune infiltration. Cox regression analysis identified seven immune cells as protective factors of BC. In the coexpression modules for DEGs of high and low immune infiltration, module 1 was related to T cells and high immune infiltration. In particular, the area under the curve (AUC) value of hub gene SASH3 was the highest, and the correlation with T cells was stronger in the high immune infiltration. Enrichment analysis found that oxidative stress, T cell aggregation, and apoptosis were observed in high immune infiltration. In addition, TP53 was identified as the most important somatic gene mutation related to immune characteristics. Importantly, we also constructed seven immune cell-based breast cancer subtypes to predict OS. Conclusion. We evaluated the immune landscape of BC and constructed the gene characteristics related to the immune landscape. The potential of T cells and SASH3 in immunotherapy of BC was revealed, which may guide the development of new clinical treatment strategies.
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Stoll, Gautier, David Enot, Bernhard Mlecnik, Jérôme Galon, Laurence Zitvogel, and Guido Kroemer. "Immune-related gene signatures predict the outcome of neoadjuvant chemotherapy." OncoImmunology 3, no. 3 (February 27, 2014): e27884. http://dx.doi.org/10.4161/onci.27884.
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Jiang, Bitao, Qingsen Sun, Yao Tong, Yuzhuo Wang, Haifen Ma, Xuefei Xia, Yu Zhou, Xingguo Zhang, Feng Gao, and Peng Shu. "An immune-related gene signature predicts prognosis of gastric cancer." Medicine 98, no. 27 (July 2019): e16273. http://dx.doi.org/10.1097/md.0000000000016273.
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Liu, K. Y. P., X. J. D. Lu, Y. Zhu, S. Yip, and C. F. Poh. "Altered Immune-Related Gene Expressions Indicate Oral Cancer Nodal Disease." Journal of Dental Research 97, no. 6 (February 28, 2018): 709–16. http://dx.doi.org/10.1177/0022034518758045.
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Lymph nodal disease (LN+) is the most significant prognostic factor of oral squamous cell carcinoma (OSCC). Current risk indicator(s) for guiding elective neck dissection (END) is insufficient for clinically node-negative (cN0) patients, resulting in under- or overtreatment. While the role of immunological events in tumorigenesis and metastasis is evident, the prognostic implication in OSCC remains unclear. The study objective was to investigate large-scale immune-related gene expression and determine its prognostic value on node-free survival (NFS). We analyzed patients who received intent-to-cure surgery with at least 3 y of follow-up and known outcome of LN through a pan-Canadian surgical trial. Total RNA was extracted from surgical tissues with >70% tumor content and analyzed on a 730-gene panel (NanoString nCounter® PanCancer Immune Panel). We first profiled gene expression in a fresh-frozen (FF) discovery set to identify differentially expressed (DE) genes, which were then used in unsupervised clustering analysis to identify patient subgroups. The prognostic value of the identified DE genes was then validated on formalin-fixed, paraffin-embedded (FFPE) samples. A total of 177 RNA samples were derived from 89 FF and 88 FFPE surgical tissues, of which 45 (51%) and 40 (45%), respectively, were from patients who developed LN+. We identified 6 DE genes overexpressed in LN+ tumors (false discovery rate <0.001; log2 fold change >1). Clustering analysis separated the patients into 2 subgroups (CM1, CM2), with CM2 exhibiting significantly increased expression and worse 5-y NFS rate (28%; P < 0.001). The prognostic value of these 6 candidate genes was validated on FFPE samples, which were also separated into 2 distinct prognostic groups, confirming the association between increased gene expression and poor 5-y NFS (CM1, 70.3%; CM2, 43.3%; P = 0.01). This is the first study identifying a panel of immune-related genes associated with NFS that can potentially be used clinically stratifying the risk of LN+ at the time of OSCC diagnosis.
Dissertations / Theses on the topic "Immune-related gene"
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Arakelian, Tsolère. "Impact of Targeting the Autophagy Related Gene Beclin 1 on the Immune Landscape of Melanoma." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS193.
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L'immunothérapie basée sur le blocage des points de contrôle immunitaire (ICBs) est un traitement prometteur pour les patients atteints de mélanome ; cependant, seule une petite sous-population en tire un bénéfice à long terme. Un des défis pour améliorer l'efficacité et étendre le bénéfice des ICBs aux patients non répondeurs est de concevoir des approches innovantes permettant de transformer les tumeurs dites "froides ou désertes pour les cellules immunitaire" en tumeurs dites "chaudes ou infiltrées par les cellules immunitaires" qui sont éligibles aux ICBs. Nous avons étudié l'impact du ciblage du gène de l'autophagie Beclin1 sur le paysage immunitaire des tumeurs de mélanome B16-F10. Nos résultats ont démonté que ce ciblage inhibait significativement la croissance tumorale B16-F10 et augmentait l'infiltration des leucocytes CD45+. Le phénotypage immunitaire a révélé une augmentation de l'infiltration de cellules NK (Natural Killer) actives, de macrophages inflammatoires et résidents de type 1, de cellules dendritiques et de lymphocytes T CD8+ actifs. L’inhibition de la croissance tumorale Becn1- n'était plus observée par la déplétion des CD8+ de l'hôte, soulignant ainsi leur rôle dans le contrôle du développement de ces tumeurs. Nos résultats ont démontré que La régulation du paysage immunitaire des tumeurs Becn1- était associée à une modulation du réseau de cytokines/chémokines dans le microenvironnement tumoral (TME). Ainsi, les tumeurs Becn1- présentaient une signature de cytokines inflammatoires (comprenant CCL5, CXCL10 et IFNg) qui pourrait être responsable de l'établissement de microenvironnement inflammatoire permissif aux cellules CD8. Nous avons révélé que la surexpression de l'IFNg dans le TME des tumeurs Becn1- était responsable de l'induction de PD-L1 sur les cellules tumorales par la voie d'activation JAK/STATs. En conclusion, cette étude met en évidence Beclin1 comme une cible majeure, capable d'induire l'infiltration des cellules effectrices immunitaires dans les mélanomes en induisant une signature inflammatoire. Elle fournit également la preuve de concept pour combiner des inhibiteurs d'autophagie avec les ICBs comme une approche de pointe pour améliorer leur efficacitéImmune Checkpoint Blockades (ICBs)-based immunotherapy has emerged as a promising treatment for melanoma patients; however only a small subset of patients reaps a long term benefit. One of the major challenges to enhance the efficacy and extend the benefit of ICBs to non-responder patients is to design innovative approaches allowing the switch of “immune desert cold tumors” to “immune infiltrated hot tumors" which are eligible for ICB-based therapies. Here, we investigated the impact of targeting the early autophagy gene Beclin1 on the immune landscape of B16-F10 melanoma tumors. We found that targeting Beclin1 (Becn1-) significantly inhibited B16-F10 tumor growth and increased the infiltration of CD45+ leukocytes into the tumor bed. Immune phenotyping revealed an increased infiltration of active Natural Killer (NK) cells, inflammatory and resident type 1 macrophages, dendritic cells, and active CD8+ T lymphocytes. The inhibition of Becn1- tumor growth was no longer observed by depleting host CD8+ T cells, thus highlighting their major role in the control of Becn1- B16-F10 tumor development. We showed that Beclin1-dependent regulation of the immune landscape was associated with profound modulation of the cytokine/chemokine network in the tumor microenvironment (TME). Importantly, we revealed that Becn1- tumors displayed an inflammatory cytokine signature (comprised, but not restricted to, CCL5, CXCL10 and IFNg) that could be responsible for the switch from cold non T-inflamed to hot T-inflamed tumors. Mechanistically, we reported that the overexpression of IFNg in Becn1- TME was responsible for the induction of Programed Death ligand-1 (PD-L1) on tumor cells through the activation of JAK/STATs pathway. Overall, this study highlights Beclin1 as a valuable target, able to drive immune effectors cells into the melanoma tumors by inducing an inflammatory signature. This study provides the proof of concept for combining drugs inhibiting early autophagy process along with ICBs as a cutting-edge approach to improve their efficacy
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Warke, Rajas V. "Molecular Dissection of the Cellular Reponse to Dengue Virus Infection." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/366.
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The immune response to viral infection involves a complexity of both innate and adaptive pathways at the cellular and the molecular level. There are many approaches to begin to define the pathways at work to control viral pathogenesis. The approach favored in this thesis was to conduct a broad screen of the innate immune response at the gene expression level of infected cells.
The innate immune response is critical to the control of viral infections. Type I interferons (IFN), IFNα and IFNβ, are antiviral proteins that are an integral part of the innate immune response. Furthermore, by virtue of their effects on maturation and activation of antigen-presenting cells, IFNs are a pivotal link between the innate and adaptive immune systems. Most cell types produce type-I IFN when exposed to viruses. However, viruses have evolved multiple strategies to suppress IFN production or signaling. It is imperative to understand the virus-host interaction at the molecular level in order to identify as yet unknown mechanisms of the host antiviral response; these additional pathways may be useful in counteracting the viral suppression of IFN. Type-I IFNs regulate expression of at least five hundred genes, suggesting a complex network of signaling pathways. Depending on the cell type different proteins regulate the induction of IFN or the expression of IFN-inducible genes. Identification of proteins that induce selected IFN-inducible genes may provide synergistic activity with or may have an advantage over type-I IFN for anti-viral therapy in the future.
Many diseases are untreatable if identified late in their progression. In resource-limited countries, many diseases are diagnosed clinically, which can lead to incorrect or delayed diagnosis and treatment. The identification of biomarkers of disease has the potential to guide the correct therapy in a timely fashion. The objective of this thesis was to identify novel anti-viral therapies and disease biomarkers for dengue virus (DENV) infection.
DENV is a mosquito-borne positive-sense single-stranded RNA virus, which causes an estimated 50 million infections annually. Most DENV infections result in a febrile illness called Dengue fever (DF). Less frequently, infections cause Dengue hemorrhagic fever (DHF), a potentially fatal vascular leakage syndrome associated with the production of pro-inflammatory cytokines. At present patients infected with DENV can only be treated by intravenous fluid support to prevent hypovolemia and hypotensive shock. This treatment is less effective in severe cases if the diagnosis is delayed. Identification of therapeutics with both antiviral and immune-modulatory activity may lower patient mortality and reduce the burden of DENV on society.
DENV infection is cleared in most individuals after a short period of viremia {Libraty, 2002 #2225}. Based on in vitro and mouse models, type-I and type-II IFN signaling pathways are thought to be critical in the regulation of DENV infection. Higher serum levels of type I and type II IFNs during acute DENV infection in patients lend support to the above hypothesis {Kurane, 1993 #2152; Libraty, 2002 #2225}.
To understand the DENV-human host cell interaction at the molecular level, we performed global gene expression analysis on DENV-infected primary human cells using Affymetrix GeneChips (HG-U133A). We studied dendritic cells (DC), monocytes, B cells and human umbilical vein endothelial cells (HUVECs), all of which are known to be permissive to DENV infection. We first identified genes commonly regulated in multiple cell types in response to DENV infection; we hypothesized that understanding this common gene expression profile would identify signaling pathways involved in regulation of viral spread, activation of immune cells or induction of inflammation. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), one of the 23 common response genes, was identified as a key link between type I and type II interferon response genes. Pretreatment of cells with recombinant TRAIL (rTRAIL) inhibited DENV replication in monocytes, B cells, HUVECs and DCs. Using the DC infection model, we showed that this inhibition of viral replication was apoptosis-independent. Type-I IFN receptor (IFNR) blocking experiments showed that signaling through the type-I IFN receptor played an important role in the antiviral activity of exogenous rTRAIL. Furthermore, TRAIL also significantly reduced the expression of mRNA and protein of pro-inflammatory cytokines (TNFα, MIP-1β and IFNα) and chemokines (MCP-2, IP-10 and IL-6) in response to DENV infection. The data that TRAIL inhibits both viral replication and pro-inflammatory cytokine production suggest that TRAIL has therapeutic value in dengue.
The endothelial cell is the site of pathology in DENV infection in vivo (vascular permeability and plasma leakage). To understand the direct effect of DENV infection on endothelial cells and its role in the induction of genes regulating vascular permeability, we compared gene expression in DENV-infected HUVECs to that of uninfected cells and cells infected with other RNA and DNA viruses, including flaviviruses (West Nile, yellow fever, and Japanese encephalitis viruses), bunyaviruses (Sin Nombre and Hantaan viruses), Epstein-Barr virus and vaccinia virus. Among the genes confirmed for their differential expression, ST2 (Interkeukin-1 receptor-like-1 protein-IL1RL1) and indoleamine 2,3-dioxygenase (IDO) were identified to be upregulated specifically in response to DENV infection. Higher serum soluble ST2 (sST2) levels were detected in DENV-infected patients than in patients with other febrile illnesses (OFI) at the end of the febrile stage and at defervescence (p=0.0088 and p=0.0004, respectively). In addition, patients with secondary DENV infections had higher serum sST2 levels compared with patients with primary DENV infections (p=0.047 at the last day of fever and p=0.030 at defervescence). Higher levels of IDO activity (pIn conclusion, global gene expression analysis identified novel proteins with promising characteristics for the treatment and/or diagnosis of DENV infection. Although further studies will be needed to validate the clinical utility of TRAIL, sST2, and IDO, these studies demonstrate the utility of this unbiased genomics approach to identify therapies to currently incurable diseases.
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Lorenzoni, Marco. "Pro-Tumorigenic role of ETS-related gene (ERG) in precursor prostate cancer lesions." Doctoral thesis, Università degli studi di Trento, 2019. http://hdl.handle.net/11572/242659.
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Prostate cancer (PCa) is the second most common cancer in men with more than 1 million new cases worldwide each year. While some of the genomic, genetic and molecular events characterizing PCa have been functionally associated with tumor onset, development and resistance to therapy, the meaning of many other molecular alterations remains poorly understood. Recent development of organoids technology and prostate organoid cultures has established an innovative and valuable model for the study of adult tissue homeostasis, physiology and disease. In this project we combined prostate organoids technology with genetic engineering and CLICK-chemistry coupled Mass Spectrometry approaches in order to better characterize molecular features of wild type and genetically engineered mouse prostate organoids modeling early steps of human prostate tumorigenesis. In details, by manipulating mPrOs to proxy ETS-related gene (ERG) precursor PIN/HGPIN lesions of human prostate, we identified possible novel pro-tumorigenic roles of ERG which unleashes cells proliferation from the tight control of growth stimuli, and, even more interesting, corrupts immune system components to escape immune surveillance. In conclusion, this project shows that coupling innovative biological systems and technological approaches can lead to significant improvements in the analysis and understanding of disease mechanisms.
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Lorenzoni, Marco. "Pro-Tumorigenic role of ETS-related gene (ERG) in precursor prostate cancer lesions." Doctoral thesis, Università degli studi di Trento, 2019. http://hdl.handle.net/11572/242659.
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Prostate cancer (PCa) is the second most common cancer in men with more than 1 million new cases worldwide each year. While some of the genomic, genetic and molecular events characterizing PCa have been functionally associated with tumor onset, development and resistance to therapy, the meaning of many other molecular alterations remains poorly understood. Recent development of organoids technology and prostate organoid cultures has established an innovative and valuable model for the study of adult tissue homeostasis, physiology and disease. In this project we combined prostate organoids technology with genetic engineering and CLICK-chemistry coupled Mass Spectrometry approaches in order to better characterize molecular features of wild type and genetically engineered mouse prostate organoids modeling early steps of human prostate tumorigenesis. In details, by manipulating mPrOs to proxy ETS-related gene (ERG) precursor PIN/HGPIN lesions of human prostate, we identified possible novel pro-tumorigenic roles of ERG which unleashes cells proliferation from the tight control of growth stimuli, and, even more interesting, corrupts immune system components to escape immune surveillance. In conclusion, this project shows that coupling innovative biological systems and technological approaches can lead to significant improvements in the analysis and understanding of disease mechanisms.
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Wong, Nai-kei. "Expression of myelin-related genes in an immune-precipitated mouse model of schizophrenia." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B4378026X.
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Wong, Nai-kei, and 黃乃淇. "Expression of myelin-related genes in an immune-precipitated mouse model of schizophrenia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4378026X.
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DiBaise, Samantha. "Decreased Expression of Immune Related Genes in the Intrauterine Growth Restricted Fetal Sheep Pancreas." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579391.
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Samuels, Veneshley. "Investigation of mycobacterial cell wall genes and their requirement for survival in immune related stressful conditions." Master's thesis, Faculty of Health Sciences, 2020. http://hdl.handle.net/11427/32963.
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Tuberculosis (TB) disease, caused by the pathogen Mycobacterium tuberculosis (Mtb), remains a major global health problem claiming 1.5-2 million lives annually. One of the major factors contributing towards Mtb's success as a pathogen is its unique cell wall and its ability to counteract various arms of the host's immune response. Understanding these survival mechanisms will help us develop new therapeutic interventions that can enhance the capacity of the immune system to kill the pathogen. A recent genome scale study profiled a list of candidate genes that are predicted to be essential for Mtb survival of host mediated responses. One candidate was ftsEX, a protein complex comprised of an ATP binding domain, FtsE, and a transmembrane domain, FtsX. FtsEX functions through interaction with a periplasmic hydrolase, RipC. FtsEX homologs in other bacteria have been linked to a key role in regulation of PG hydrolysis during elongation and division. Using M. smegmatis as a model, we hypothesised that FtsEX and RipC are required in the regulation of PG hydrolysis during normal cell wall elongation and division under stressful conditions in vitro. Antibiotic sensitivity was confirmed using Alamar blue MIC determination assays, which showed that ftsEX and ripC had increased sensitivity to chloramphenicol and not to rifampicin, isoniazid and ethambutol. Our growth curve analysis showed that ftsEX and ripC are not essential for survival in normal growth conditions. However, ftsEX and ripC are conditionally essential for M. smegmatis in low salt media. Growth defects in this condition were characterized by short and bulgy cells, as well as elongated filamentous cells with visible chaining. Major morphological changes were seen under nitrosative stress. A higher proportion of cells struggled to divide normally and formed chains. Lateral branching was also observed in ΔftsE, ΔftsX and ΔftsEX but not in ΔripC. The protein complex was also required for survival in media containing rifampicin. Treatment with the drug exacerbated growth defects of all the mutants, which were much shorter than WT cells, indicating impairment in the elongation process. Collectively, mutants are much shorter in length with an exception of a few extremely lengthy cells, suggesting that ftsEX and ripC are required for both normal cell elongation and division and ultimately for survival in stressful conditions.
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Paues, Jakob. "Brain Stem Involvement in Immune and Aversive Challenge." Doctoral thesis, Linköping : Linköping University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7579.
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Lourenço, Anete Pedro. "Genes codificadores dos peptídeos antimicrobianos e de outras proteínas envolvidas na resposta imune de in Apis mellifera." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-04042008-144240/.
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Os insetos desenvolveram um sistema imune eficiente contra parasitas e patógenos, que compreende a resposta celular e a humoral. Os mecanismos celulares envolvem a fagocitose e a encapsulação pelos hemócitos, enquanto que as respostas humorais incluem a ativação da Profenoloxidase, e a síntese pelo corpo gorduroso dos peptídeos antimicrobianos, que são liberados na hemolinfa. Duas vias de sinalização intracelular, Toll e Imd, controlam a expressão dos genes codificadores dos peptídeos antimicrobianos. A análise do Genoma da abelha Apis mellifera permitiu a identificação dos genes dessas vias. No entanto, pouco se conhece do mecanismo de resposta imune nessas abelhas. Desta maneira, nos propusemos analisar a transcrição de genes efetores da resposta imune (abaecina, hymenoptaecina, defensina, transferrina, profenoloxidase), assim como os genes integrantes das vias de sinalização, tais como os genes de reconhecimento de microorganismos (PGRP, GNBP) e ainda, os de sinalização (cactus, relish, dorsal 1-B). Avaliamos também possíveis proteínas implicadas na resposta imune, como as proteínas de estocagem Vitelogenina, Hexamerina 70a, Lipoforina I/II e Lipoforina III. Finalmente, analisamos o efeito da nutrição e do envelhecimento sobre a imunidade em abelhas. Para análise da expressão dos genes das vias de sinalização, as abelhas foram infectadas com bactérias Serratia marcescens ou Micrococcus luteus por injeção ou via alimentação. A infecção com esses microorganismos provocou a transcrição de peptídeos antimicrobianos e de transferrina em altas quantidades após 3 e 12 horas de tratamento, além da alteração na quantidade de transcritos de outros genes. O papel dos genes profenoloxidase e dorsal na imunidade, descritos como codificadores de importantes proteínas em outros insetos, foi avaliado através da metodologia de silenciamento gênico por RNA de interferência. Observamos a diminuição da transcrição do gene alvo, mostrando a eficiência da metodologia. No entanto, a simples injeção de um RNA de fita dupla foi capaz de ativar o sistema imune de abelhas. Este efeito contribuiu para a dificuldade de atribuição do papel da Profenoloxidase na imunidade de abelhas. Contudo, os resultados de silenciamento de dorsal e suas isoformas, nos levaram a considerar que dorsal 1-A ou dorsal 2 participam da via de sinalização intracelular para produção de peptídeos antimicrobianos, principalmente de defensina. Em relação às proteínas de estocagem, tanto a quantidade de transcritos quanto de proteínas diminui após infecção com bactérias, indicando que estas proteínas estão envolvidas de alguma forma no processo de imunidade em abelhas. Além disso, consumo de alimentos ricos em proteína aumentou os níveis de transcritos das proteínas de estocagem, o que muito provavelmente favorece a manutenção da capacidade de resposta imune de abelhas. O efeito do envelhecimento no declínio da imunidade foi analisado em abelhas nutridoras (novas) e forrageiras (velhas) de uma colônia típica. Além disso, foram utilizadas abelhas de uma colônia single-cohort, que eram de uma mesma idade, mas algumas eram nutridoras, enquanto outras eram forrageiras. Todas as abelhas, independentemente da idade ou comportamento, foram capazes de ativar o sistema imune após infecção pela bactéria S. marcescens. No entanto, as abelhas com o comportamento de forrageira, independentemente da idade, sempre foram mais susceptíveis a infecções que as nutridoras. Este fato se deve, muito provavelmente, às diferenças fisiológicas entre essas abelhas, que proporciona às nutridoras maior competência à sobrevivência.Insects have developed an efficient immune system against parasites and pathogens, which is comprised of both cellular and humoral responses. The cellular mechanisms involve phagocytosis and encapsulation by hemocytes, whereas the humoral responses include activation of prophenoloxidase and synthesis of antimicrobial peptides by the fat body, which are released into the hemolymph. Two signaling pathways, Toll and Imd, control the expression of genes encoding antimicrobial peptides. Genome-wide analyses of the honey bee, Apis mellifera, have identified predicted genes for these signaling pathways. However, immune response mechanisms in honey bees were not yet in depth studied. We analyzed the transcription of effector genes (abaecin, hymenoptaecin, defensin, transferin, prophenoloxidase), as well as other immune genes, such as pathogen recognition genes (PGRP, GNBP) and signaling genes (cactus, relish, dorsal 1- B). We also investigated the role of the storage proteins Vitellogenin, Hexamerin 70a, Lipophorin I/II and Lipophorin III in the honey bee immunity. Finally, we analyzed the effect of nutrition and aging on honey bee immunity. Gene expression of signaling pathway components was assessed in honey bees that had been infected with the bacteria Serratia marcescens or Micrococcus luteus through injection or oral challenge. Honey bees infected with these microorganisms had strong up-regulation of antimicrobial peptide genes and of transferin, and also other changes in transcript abundance after 3 and 12 hours of challenge. The roles of prophenoloxidase and dorsal in the immune response, described as genes encoding important proteins in other insects, were also investigated. In this case we used RNA interference (RNAi) to silence the expression of these genes. RNAi efficiently silenced the target genes. However, injection of doublestranded RNA in honey bees induced a reaction by the immune system. This made it difficult to determine the role of prophenoloxidase in honey bee immunity. Yet, silencing of dorsal and its isoforms led us to consider dorsal 1-A or dorsal 2 as members of the signaling pathways that produce antimicrobial peptides, especially defensin. The abundance of storage proteins transcripts and proteins was lower in infected bees than in controls, giving evidence that these proteins participate in the immune process in honey bees. Moreover, protein consumption caused up-regulation of genes encoding storage proteins, which may favor the maintenace of the immune response capacity. The effect of aging on decline in immunity was analyzed in (young) nurse bees and (old) foragers from normal free-flying colony. We also examined bees from a single-cohort colony, in which all individuals were at the same age; but some were nursing, while others were foraging. All the bees, independent of age or behavior, were able to activate the immune system after infection with S. marcescens. However, foragers, independent of age, were always more susceptible to infections than were nurse bees. This is probably due to physiological differences between bees, which confers to the nurses more competence to survivorship.
Books on the topic "Immune-related gene"
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Sousek, Alexandra, and Mehdi Tafti. The genetics of sleep. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0005.
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Although there is strong evidence for a genetic contribution to inter-individual variations in sleep, the underlying factors and their interaction remain largely elusive. Much effort has been expended in studying genetic variations contributing to circadian and sleep phenotypes, the individual pattern of the human sleep EEG, reactions to sleep loss, and the pathophysiology of sleep-related disorders. Certain sleep-related diseases may be caused by single genes, while the etiology of others seems to be variable and complex. This is especially the case when the immune system is involved. This chapter reports on twin and familial studies, genetic variations and mutations affecting neurotransmitters and other signaling pathways and thereby affecting sleep, and impacts of gene expression processes and the immune system on sleep. Although much knowledge has been gained, further research is needed to elucidate the all-embracing mechanisms and their interactions that regulate sleep.
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Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.
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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
Book chapters on the topic "Immune-related gene"
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Kim, D. K., Y. H. Hong, D. W. Park, S. J. Lamont, and H. S. Lillehoj. "Differential Immune-related Gene Expression in Two Genetically Disparate Chicken Lines during Infection by Eimeria maxima." In Animal Genomics for Animal Health, 131–40. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000317153.
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Sadiq, Alia, Nonhlanhla P. Khumalo, and Ardeshir Bayat. "Genetics of Keloid Scarring." In Textbook on Scar Management, 61–76. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_8.
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AbstractKeloid disease is a benign fibro-proliferative reticular dermal tumor that develops in response to dysregulated cutaneous wound-healing process. The key alterations result in keloid formation have not been fully understood yet.Extensive literature review suggests that there is a strong genetic predisposition for keloid formation as keloid cases have appeared in twins, families, Asian and African descendant ethnic groups predominantly. Thus, there have been several attempts to investigate the genetic variations that may act as contributing factors in keloid pathogenesis, but no single genetic cause has been identified so far. Gene expression studies have shown highly variable results in linkage analysis of keloid families and in keloid fibroblasts. These findings provide clues that keloids arise from heterogeneous genetic events in coordination with immune-related components for example, the Major Histocompatibility Complex genes, consequently that may contributing towards dermal fibrosis. In addition, it is likely that multiple genetic and epigenetic factors are responsible for the development of the disease pathology. In summary, keloid disease is a disorder in which the exact genetic contribution to pathogenesis is yet to be elucidated. Understanding the genetic basis of keloid disease would help to identify targeted therapies as well as accurately assess individual genetic susceptibility to keloids, in order to provide a more personalized approach to their management.
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Harris, R. Adron, and Yuri A. Blednov. "Neuroimmune Genes and Alcohol Drinking Behavior." In Neural-Immune Interactions in Brain Function and Alcohol Related Disorders, 425–40. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4729-0_13.
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Hirono, Ikuo, and Takashi Aoki. "Immune-related genes of the Japanese flounder, Paralichthys olivaceus." In Aquatic Genomics, 286–300. Tokyo: Springer Japan, 2003. http://dx.doi.org/10.1007/978-4-431-65938-9_26.
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Wang, Yishu, Lingyun Xu, Xuehan Tian, and Zhe Lin. "Identification of Gastric Cancer Immune Microenvironment Related Genes with Poor Prognosis and Tumor Immune Infiltration." In Bioinformatics Research and Applications, 142–52. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-91415-8_13.
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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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Koren, E., H. Zhou, A. Cahaner, E. D. Heller, J. Pitcovski, and S. J. Lamont. "Unique Co-expression of Immune Cell-related Genes in IBDV Resistant Chickens Indicates the Activation of Specific Cellular Host-response Mechanisms." In Animal Genomics for Animal Health, 153–59. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000317155.
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Young Cheon, Na, Subin Kim, and Ja Yil Lee. "Biophysical and Biochemical Approaches for R-Loop Sensing Mechanism." In Gene Expression [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103176.
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An R-loop is a triple-stranded nucleic acid structure consisting of a DNA–RNA hybrid and a displaced single-stranded DNA. R-loops are associated with diverse biological reactions, such as immune responses and gene regulation, and dysregulated R-loops can cause genomic instability and replication stress. Therefore, investigating the formation, regulation, and elimination of R-loops is important for understanding the molecular mechanisms underlying biological processes and diseases related to R-loops. Existing research has primarily focused on R-loop detection. In this chapter, we introduce a variety of biochemical and biophysical techniques for R-loop sensing and visualization both in vivo and in vitro, including single-molecule imaging. These methods can be used to investigate molecular mechanisms underlying R-loop search and identification.
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"An Emerging Role for Calcitonin Gene-Related Peptide in Regulating Immune and Inflammatory Functions." In Autonomic Neuroimmunology, 113–28. CRC Press, 2003. http://dx.doi.org/10.3109/9780203008966-10.
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Karthikeyan, Kesavan, Nivedita Gautam, Olivia Parra-Marín, and Selvasankar Murugesan. "Gene Therapy: A New Avenue for the Management of Ophthalmic Diseases." In Nanoparticles and Nanocarriers-Based Pharmaceutical Formulations, 395–435. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815049787122010016.
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Gene therapy aims at intercellular delivery of functional genetic material to the affected area to restore its function or block a dysfunctional gene using viral vectors (Adeno-associated virus) or non-viral vectors (liposomes, SLNs). Gene therapy for the management of ocular diseases is emerging with improved and encouraging results. The Eye has well-defined anatomy, tight ocular barriers, and immune-privileged. It is a perfect target for gene therapy. Recently, many clinical trials are underway or have been completed. The success of these clinical trials promotes the treatment of several ocular diseases (Age-related macular degeneration, glaucoma, retinitis pigmentosa, and choroideremia). Gene therapy should possess an efficient targeting capacity and longstanding gene expression. Viral vectors are mainly used for gene therapy, but due to the risk associated with immunogenicity and mutagenesis, non-viral vectors are widely utilized. This chapter summarizes the recent development of therapeutic gene delivery approaches for the effective management of ocular diseases and their use in ophthalmology.
Conference papers on the topic "Immune-related gene"
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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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Nygaard, Vigdis, Vegar J. Dagenborg, Olga Østrup, Einar A. Rødland, Veronica Skarpeteig, Laxmi Silwal-Pandit, Krzysztof Grzyb, et al. "Abstract 1752: Immune-related gene signatures in colorectal liver metastases: Exposing an opportunity for immune modulating therapy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1752.
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Tarhini, Ahmad A., Yan Lin, Hui-Min Lin, Cindy Sander, William A. La Framboise, and John M. Kirkwood. "Abstract 2911: Immune related melanoma gene expression profile predicts neoadjuvant ipilimumab clinical benefit." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2911.
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Araujo, Jhajaira M., Luis E. Raez, Christian D. Rolfo, Luis J. Schwarz, Ulises Infante-Huaytalla, Kevin J. Paez, Luis R. García, et al. "Abstract 1518: Gene expression profile and gender differences related with immune processes in solid tumors." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1518.
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Araujo, Jhajaira M., Luis E. Raez, Christian D. Rolfo, Luis J. Schwarz, Ulises Infante-Huaytalla, Kevin J. Paez, Luis R. García, et al. "Abstract 1518: Gene expression profile and gender differences related with immune processes in solid tumors." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1518.
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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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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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Kim, J.-Y., HH Jung, JE Lim, EY Cho, SK Lee, JH Yu, JE Lee, et al. "Abstract P4-08-30: Prognostication of immune related gene expression in patients with triple negative breast cancer." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p4-08-30.
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Wang, Z., X. Wei, L. Ye, and Q. Zhou. "Validation of an Immune Related Gene Pair Index as a Prognostic Marker of Lung Squamous Cell Carcinoma." 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.a6177.
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Fremd, C., N. Halama, R. Wirtz, I. Zoernig, H.-P. Sinn, Z. Varga, M. Feisst, et al. "Abstract P4-06-10: Immune related gene expression to explore immue escape in primary to metastatic breast cancer transition." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p4-06-10.
Full textReports on the topic "Immune-related gene"
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Sauer, Zachary C., Michael G. Kaiser, and Susan J. Lamont. Chicken Immune-related Gene Expression after Stimulation with Bacterial Component. Ames (Iowa): Iowa State University, January 2015. http://dx.doi.org/10.31274/ans_air-180814-1320.
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Sandford, Erin, Ceren Ciraci, Behnam Abasht, Jack C. M. Dekkers, and Susan J. Lamont. SNPs in Region of NF-Kappa-B Gene Associated with Expression of Immune-Related Genes. Ames (Iowa): Iowa State University, January 2010. http://dx.doi.org/10.31274/ans_air-180814-95.
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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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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.
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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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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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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.
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Perk, Shimon, Maricarmen Garcia, Alexander Panshin, Caroline Banet-Noach, Irina Gissin, Mark W. Jackwood, and David Stallknecht. Avian Influenza Virus H9N2: Characterization and Control Strategies. United States Department of Agriculture, June 2007. http://dx.doi.org/10.32747/2007.7709882.bard.
Full textAbstract:
Control of Avian Influenza (AI) infection is a highly topical subject of major economicimportance for the worldwide poultry industry at the national level and for international trade.H9N2 viruses are endemic in poultry throughout Asia and the Middle East, causing major losses inproduction. Moreover, these viruses pose wider threats since they have been isolated from bothswine and humans. At the same time, study of the AI viruses affords an opportunity to explore anumber of problems of intriguing scientific interest. The overall goal of this project was to developa sound control strategy for avian influenza subtype H9N2 viruses (AI H9N2) in commercialpoultry in Israel. The one-year feasibility study focused on two main goals, namely: to study themolecular characteristics of AI H9N2 circulating during the last seven years in Israel and todevelop tools enabling differentiation between the immune response to vaccination and infectionwith H9N2.Genetic and phylogenetic characterization of 29 selected AI H9N2 isolates (2000-2006)was performed by complete sequencing of hemagglutinin (HA), neuraminidase (NA), and all sixinternal genes [nucleoprotein (NP), polymerase basic 1 (PB1), polymerase basic 2 (PB2),polymerase acid (PA), matrix (M), and nonstructural (NS) genes]; comparative phylogenetic andgenetic analyses of these sequences; and comparative genetic analyses of deduced amino acidsequences of the HA, NA, NS1, and NS2 proteins. The major conclusions of the molecularanalyses were: (1) Israeli isolates, together with other H9N2 viruses isolated in Middle Eastcountries, comprise a single regional sublineage related to the G1-lineage. In addition, Israeliisolates subdivided into three different subgroups. Genetic analysis of these viruses suggests thatthey underwent divergent evolution paths.
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Brown Horowitz, Sigal, Eric L. Davis, and Axel Elling. Dissecting interactions between root-knot nematode effectors and lipid signaling involved in plant defense. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598167.bard.
Full textAbstract:
Root-knot nematodes, Meloidogynespp., are extremely destructive pathogens with a cosmopolitan distribution and a host range that affects most crops. Safety and environmental concerns related to the toxicity of nematicides along with a lack of natural resistance sources threaten most crops in Israel and the U.S. This emphasizes the need to identify genes and signal mechanisms that could provide novel nematode control tactics and resistance breeding targets. The sedentary root-knot nematode (RKN) Meloidogynespp. secrete effectors in a spatial and temporal manner to interfere with and mimic multiple physiological and morphological mechanisms, leading to modifications and reprogramming of the host cells' functions, resulted in construction and maintenance of nematodes' feeding sites. For successful parasitism, many effectors act as immunomodulators, aimed to manipulate and suppress immune defense signaling triggered upon nematode invasion. Plant development and defense rely mainly on hormone regulation. Herein, a metabolomic profiling of oxylipins and hormones composition of tomato roots were performed using LC-MS/MS, indicating a fluctuation in oxylipins profile in a compatible interaction. Moreover, further attention was given to uncover the implication of WRKYs transcription factors in regulating nematode development. In addition, in order to identify genes that might interact with the lipidomic defense pathway induced by oxylipins, a RNAseq was performed by exposing M. javanicasecond-stage juveniles to tomato protoplast, 9-HOT and 13-KOD oxylipins. This transcriptome generated a total of 4682 differentially expressed genes (DEGs). Being interested in effectors, we seek for DEGs carrying a predicted secretion signal peptide. Among the DEGs including signal peptide, several had homology with known effectors in other nematode species, other unknown potentially secreted proteins may have a role as root-knot nematodes' effectors which might interact with lipid signaling. The molecular interaction of LOX proteins with the Cyst nematode effectors illustrate the nematode strategy in manipulating plant lipid signals. The function of several other effectors in manipulating plant defense signals, as well as lipids signals, weakening cell walls, attenuating feeding site function and development are still being studied in depth for several novel effectors. As direct outcome of this project, the accumulating findings will be utilized to improve our understanding of the mechanisms governing critical life-cycle phases of the parasitic M. incognita RKN, thereby facilitating design of effective controls based on perturbation of nematode behavior—without producing harmful side effects. The knowledge from this study will promote genome editing strategies aimed at developing nematode resistance in tomato and other nematode-susceptible crop species in Israel and the United States.