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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.
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Mikhailova, Svetlana V., and Dinara E. Ivanoshchuk. "Innate-Immunity Genes in Obesity." Journal of Personalized Medicine 11, no. 11 (November 14, 2021): 1201. http://dx.doi.org/10.3390/jpm11111201.
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The main functions of adipose tissue are thought to be storage and mobilization of the body’s energy reserves, active and passive thermoregulation, participation in the spatial organization of internal organs, protection of the body from lipotoxicity, and ectopic lipid deposition. After the discovery of adipokines, the endocrine function was added to the above list, and after the identification of crosstalk between adipocytes and immune cells, an immune function was suggested. Nonetheless, it turned out that the mechanisms underlying mutual regulatory relations of adipocytes, preadipocytes, immune cells, and their microenvironment are complex and redundant at many levels. One possible way to elucidate the picture of adipose-tissue regulation is to determine genetic variants correlating with obesity. In this review, we examine various aspects of adipose-tissue involvement in innate immune responses as well as variants of immune-response genes associated with obesity.
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Tsuchiya, Naoyuki, Jun Ohashi, and Katsushi Tokunaga. "Variations in immune response genes and their associations with multifactorial immune disorders." Immunological Reviews 190, no. 1 (December 2002): 169–81. http://dx.doi.org/10.1034/j.1600-065x.2002.19013.x.
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Meeks, Michael D., Terri K. Wade, Ronald K. Taylor, and William F. Wade. "Immune Response Genes Modulate Serologic Responses to Vibrio cholerae TcpA Pilin Peptides." Infection and Immunity 69, no. 12 (December 1, 2001): 7687–94. http://dx.doi.org/10.1128/iai.69.12.7687-7694.2001.
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ABSTRACT Cholera is an enteric disease caused by Vibrio cholerae. Toxin-coregulated pilus (TCP), a type 4 pilus expressed by V. cholerae, is a cholera virulence factor that is required for host colonization. The TCP polymer is composed of subunits of TcpA pilin. Antibodies directed against TcpA are protective in animal models of cholera. While natural or recombinant forms of TcpA are difficult to purify to homogeneity, it is anticipated that synthesized TcpA peptides might serve as immunogens in a subunit vaccine. We wanted to assess the potential for effects of the immune response (Ir) gene that could complicate a peptide-based vaccine. Using a panel of mice congenic at the H-2 locus we tested the immunogenicity of TcpA peptide sequences (peptides 4 to 6) found in the carboxyl termini of both the classical (Cl) and El Tor (ET) biotypes of TCP. Cl peptides have been shown to be immunogenic in CD-1 mice. Our data clearly establish that there are effects of the Ir gene associated with both biotypes of TcpA. These effects are dynamic and dependent on the biotype of TcpA and the haplotypes of the host. In addition to the effects of the classic class II Ir gene, class I (D, L) or nonclassical class I (Qa-2) may also affect immune responses to TcpA peptides. To overcome the effects of the class II Ir gene, multiple TcpA peptides similar to peptides 4, 5, and 6 could be used in a subunit vaccine formulation. Identification of the most protective B-cell epitopes of TcpA within a particular peptide and conjugation to a universal carrier may be the most effective method to eliminate the effects of the class II and class I Ir genes.
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worku, Mulumebet, Bahrath Kumar, and Hamid Ismail. "Differential Expression of Cow Innate and Adaptive Responses Genes in Response to Eugenol." Journal of Animal Science 99, Supplement_2 (May 1, 2021): 31–32. http://dx.doi.org/10.1093/jas/skab096.056.
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Abstract Dietary phytochemicals have both nutritional and health benefits for farm animals. Research on the immunomodulatory effects of phytochemicals may aid in developing novel therapeutic agents and provide insights into the regulation of gene expression. Eugenol (4-allyl-2-methoxyphenyl) is the active ingredient in clove oil that has been studied for its immunomodulatory/anti-inflammatory effects. The objective of this study was to evaluate the effect of eugenol on the expression of genes associated with the cow’s innate and adaptive immune responses. Blood was collected from (n = 3) clinically healthy Holstein-Friesian cows from the North Carolina A&T State University Dairy Unit. One milliliter of whole blood from three cows was treated individually with 10 ng/mL of Eugenol (Sigma-Aldrich St. Louis, MO), or maintained in PBS, incubated at 37ºC for 30 minutes. Total RNA was extracted, reverse transcribed, and real-time PCR was carried out using the RT2 Profiler™ human Innate & Adaptive Immune Responses PCR Array containing 84 genes, as recommended by the manufacturer (Qiagen). The Livak method was used to calculate fold change (FC >2 considered significant). The analysis showed that 25 genes out of 84 genes were affected by treatment with eugenol. Among 25 genes, 19 were upregulated, and 2 genes were downregulated. The highest up-regulated and down-regulated genes following exposure to eugenol was IL23A and Interferon Regulatory Factor 7 (IRF7), respectively. The upregulation of the IL-23A gene expression by exogenous eugenol may be important in the production of pro-inflammatory cytokines and warrants further studies to investigate the mechanism involved. Interferon Regulatory Factor 7 is a critical regulator of type I interferon production and plays an important role in innate immune responses. The observed transcriptional expression of IL23A and IRF7 by eugenol provides an insight into immune modulation in cow blood.
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Inman, R. D. "Immunogenetic aspects of host immune response." Canadian Journal of Microbiology 34, no. 3 (March 1, 1988): 319–22. http://dx.doi.org/10.1139/m88-058.
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The central role of histocompatibility leukocyte antigens (HLA) class II molecules in antigen presentation has received great attention in recent years, yet class I molecules have been defined as primarily functioning as a restriction element for cytotoxic T cell killing of virus-infected cells. Extensive clinical evidence, however, indicates that the HLA class I genes are strongly associated with nonseptic complications of enteric and genitourinary bacterial infections. Ninety percent of patients with Reiter's syndrome and reactive arthritis are positive for HLA-B27, yet the mechanism of disease susceptibility conferred by this gene remains obscure. Hypotheses concerning this interaction include (i) class I antigens functioning as receptors for microbial antigens; (ii) class I antigens expressing determinants that cross-react with microbial antigens; and (iii) class I genes controlling immunoregulatory functions that dictate qualitative differences in immune response to pathogenic organisms. These hypotheses await formal testing and hold great promise for understanding immunogenetic control of immune responses in general.
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Fijarczyk, Anna, Katarzyna Dudek, Marta Niedzicka, and Wiesław Babik. "Balancing selection and introgression of newt immune-response genes." Proceedings of the Royal Society B: Biological Sciences 285, no. 1884 (August 15, 2018): 20180819. http://dx.doi.org/10.1098/rspb.2018.0819.
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The importance of interspecific introgression as a source of adaptive variation is increasingly recognized. Theory predicts that beneficial genetic variants cross species boundaries easily even when interspecific hybridization is rare and gene flow is strongly constrained throughout the genome. However, it remains unclear whether certain classes of genes are particularly prone to adaptive introgression. Genes affected by balancing selection (BS) may constitute such a class, because forms of BS that favour novel, initially rare alleles, should facilitate introgression. We tested this hypothesis in hybridizing newts by comparing 13 genes with signatures of BS, in particular an excess of common non-synonymous polymorphisms, to the genomic background (154 genes). Parapatric hybridizing taxa were less differentiated in BS candidate genes than more closely related allopatric lineages, while the opposite was observed in the control genes. Coalescent and forward simulations that explored neutral and BS scenarios under isolation and migration showed that processes other than differential gene flow are unlikely to account for this pattern. We conclude that BS, probably involving a form of novel allele advantage, promotes introgression. This mechanism may be a source of adaptively relevant variation in hybridizing species over prolonged periods.
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Kumar, Neeraj, Gurvinder Kaur, and Narinder Mehra. "Genetic determinants of Type 1 diabetes: immune response genes." Biomarkers in Medicine 3, no. 2 (April 2009): 153–73. http://dx.doi.org/10.2217/bmm.09.7.
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Howell, M. D., B. E. Kim, and D. Y. Leung. "Immunomodulatory Effect of Rapamycin on Innate Immune Response Genes." Journal of Allergy and Clinical Immunology 123, no. 2 (February 2009): S33. http://dx.doi.org/10.1016/j.jaci.2008.12.1070.
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Shleptsova, V. A., E. V. Trushkin, O. A. Bystryh, J. I. Davydov, N. P. Obrazcova, E. S. Grebenuk, and A. G. Tonevitsky. "Expression of Early Immune Response Genes during Physical Exercise." Bulletin of Experimental Biology and Medicine 149, no. 1 (June 17, 2010): 89–92. http://dx.doi.org/10.1007/s10517-010-0883-6.
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Nepom, Gerald T. "The Effects of Variations in Human Immune-Response Genes." New England Journal of Medicine 321, no. 11 (September 14, 1989): 751–52. http://dx.doi.org/10.1056/nejm198909143211108.
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Pignata, Claudio, and Rosa Romano. "In This Issue: FOX Genes and the Immune Response." International Reviews of Immunology 33, no. 2 (March 4, 2014): 81–82. http://dx.doi.org/10.3109/08830185.2014.887827.
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Mehta, Akash M., Merel Mooij, Ivan Branković, Sander Ouburg, Servaas A. Morré, and Ekaterina S. Jordanova. "Cervical Carcinogenesis and Immune Response Gene Polymorphisms: A Review." Journal of Immunology Research 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/8913860.
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The local immune response is considered a key determinant in cervical carcinogenesis after persistent infection with oncogenic, high-risk human papillomavirus (HPV) infections. Genetic variation in various immune response genes has been shown to influence risk of developing cervical cancer, as well as progression and survival among cervical cancer patients. We reviewed the literature on associations of immunogenetic single nucleotide polymorphism, allele, genotype, and haplotype distributions with risk and progression of cervical cancer. Studies on HLA and KIR gene polymorphisms were excluded due to the abundance on literature on that subject. We show that multiple genes and loci are associated with variation in risk of cervical cancer. Rather than one single gene being responsible for cervical carcinogenesis, we postulate that variations in the different immune response genes lead to subtle differences in the effectiveness of the antiviral and antitumour immune responses, ultimately leading to differences in risk of developing cervical cancer and progressive disease after HPV infection.
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Jin, Lei, Lin Deng, and Wanchun Wang. "Candidate Genes of Allergic Dermatitis Are Associated with Immune Response." Journal of Healthcare Engineering 2022 (January 4, 2022): 1–11. http://dx.doi.org/10.1155/2022/8745722.
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Allergic dermatitis (AD) is a common and burdensome inflammatory skin disease, and diagnosis is challenging. This study was conducted to identify candidate genes for AD diagnosis and underlying molecular mechanisms. Gene expression profiles were obtained from datasets GSE121212, GSE130588, and GSE157194. Use differential analysis to identify differentially expressed genes (DEGs) between AD and control. Use enrichment analysis to identify potential molecular dysregulation mechanisms. Comprehensive least absolute shrinkage and selection operator (LASSO) logistic regression, receiver operator characteristic (ROC) curve, and logistic regression analysis are used to identify candidate genes. In addition, ssGSEA and ImmPort database were used to identify AD-related immune response abnormalities. In this study, a total of 60 common genes were identified. Enrichment analysis found that these genes are mainly involved in Th17 cell immune and complement and coagulation cascades. LASSO regression analysis identified 18 feature genes, and screened genes with AUC >0.75 were selected as candidate genes. Finally, PLA2G4D, IFI6, AGR3, IGFL1, SPRR3, ATP13A5, SERPINB13, KRT16, HAS3, and CH25H were recognized as candidate genes and may be able to diagnose AD. PLA2G4D, CH25H, and IFI6 may be risk factors for AD based on logistic analysis. Furthermore, we identified the abnormalities of immune response activation in AD patients. Interestingly, PLA2G4D, CH25H, and IFI6 had positive correlations with immune cells and signaling pathways. PLA2G4D, CH25H, and IFI6 may be candidate diagnostic genes for AD. This may be related to their promotion of abnormal immune activation, especially Th17 cell immune.
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NAJİ, Ahmed Qasim, Md Mahmodul Hasan SOHEL, Saif Adil Abbood AL-JANABİ, Ghulam Asghar SAJİD, and Mehmet Ulaş ÇINAR. "Akkaraman ve Romanov Kuzularının Alveolar Makrofajlarında Lipopolisakkarit ve Lipoteikoik Asite Yanıtta İmmün İlişkili Genlerin Ekspresyon Profilinin Araştırılması." Hayvan Bilimi ve Ürünleri Dergisi 5, no. 1 (June 28, 2022): 7–23. http://dx.doi.org/10.51970/jasp.1050658.
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The alveolar macrophages (AMs) are frontier of defense against foreign materials that initiate immune response in lungs. Knowledge of the expression dynamics of major immune-related genes in the alveolar macrophages in response to lipopolysaccharide (LPS) and lipoteichoic acid (LTA) challenge can help to understand disease mechanism involved in several respiratory diseases. The aim of this study was to investigate the mRNA expression of selected immune-related genes in response to lipopolysaccharide (LPS) and lipoteichoic acid (LTA) challenge in sheep alveolar macrophages in vivo. Results revealed that Romanov lambs exhibited higher mRNA expression of TLR2, TLR4, NF-ĸβ, TNFα, IL-1β, IL-6, IL-8, and IL-10 genes as compared to Akkaraman lambs along with the control of all treatments. Moreover, the expression of TLR2, TLR4, NF-ĸβ, TNFα, IL-1β, IL-6, IL-8, and IL-10 genes was higher in combine treatment of LPS and LTA as compared to separate treatments of LPS and LTA in both breeds. The results showed that the mRNA expression of immune-related genes was significantly increased in the sheep AMs in response to LPS and LTA treatment whereas a synergistic effect was observed in LPS+LTS treatment. Also, breed comparison showed that the native Akkaraman was more resistant to disease compared to exotic Romanov.
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Fathi, Moataz, Ibrahim Al-Homidan, Gamal Rayan, Salah El-Safty, Tarek Ebeid, and Osama Abou-Emera. "Laying performance, immune response and antioxidant properties of hens segregating for naked neck and frizzle genes under low ambient temperature." Czech Journal of Animal Science 64, No. 5 (May 26, 2019): 216–25. http://dx.doi.org/10.17221/221/2018-cjas.
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Major genes could be introgressed into laying hens to attenuate heat stress. However, under cold and/or moderate ambient temperature, these genes might possess different behaviour. The main objective of this study was to evaluate laying performance, immune response, and antioxidant status of native laying hens segregating for naked neck (Na) and frizzle (F) genes under low ambient temperature. Five genotypes were studied: homozygous naked neck (NaNaff), heterozygous naked neck (Nanaff), homozygous frizzle (nanaFF), heterozygous frizzle (nanaFf), and normally feathered (nanaff). The hens were raised under temperature range 22.2–16.7°C. No adverse effect due to ambient temperature was detected in laying performance for naked neck genotypes. Significant decrease in egg weight was recorded in nanaFF genotype compared to the other genotypes leading to significant decrease in egg mass. Significant improvement in shell thickness was associated with Na and F genes. NaNaff genotype had a significantly higher eggshell strength compared to nanaff. Furthermore, Na and F genes improved cellular mediated immune responsiveness, whereas this improvement did not extend to humoral immunity. Birds carrying F gene in homozygous state had a higher total antioxidant activity compared to the remaining genotypes. It could be concluded that the presence of Na and F genes in laying hens raised under low ambient temperature significantly increased shell thickness and, in turn, improved shell strength. Moreover, they greatly enhanced cellular immunity, particularly in heterozygous naked neck status.
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Alper, Scott, Sandra J. McBride, Brad Lackford, Jonathan H. Freedman, and David A. Schwartz. "Specificity and Complexity of the Caenorhabditis elegans Innate Immune Response." Molecular and Cellular Biology 27, no. 15 (May 25, 2007): 5544–53. http://dx.doi.org/10.1128/mcb.02070-06.
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ABSTRACT In response to infection, Caenorhabditis elegans produces an array of antimicrobial proteins. To understand the C. elegans immune response, we have investigated the regulation of a large, representative sample of candidate antimicrobial genes. We found that all these putative antimicrobial genes are expressed in tissues exposed to the environment, a position from which they can ward off infection. Using RNA interference to inhibit the function of immune signaling pathways in C. elegans, we found that different immune response pathways regulate expression of distinct but overlapping sets of antimicrobial genes. We also show that different bacterial pathogens regulate distinct but overlapping sets of antimicrobial genes. The patterns of genes induced by pathogens do not coincide with any single immune signaling pathway. Thus, even in this simple model system for innate immunity, striking specificity and complexity exist in the immune response. The unique patterns of antimicrobial gene expression observed when C. elegans is exposed to different pathogens or when different immune signaling pathways are perturbed suggest that a large set of yet to be identified pathogen recognition receptors (PRRs) exist in the nematode. These PRRs must interact in a complicated fashion to induce a unique set of antimicrobial genes. We also propose the existence of an “antimicrobial fingerprint,” which will aid in assigning newly identified C. elegans innate immunity genes to known immune signaling pathways.
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Gururajan, Murali, Alan Simmons, Trivikram Dasu, Brett T. Spear, Christopher Calulot, Darrell A. Robertson, David L. Wiest, John G. Monroe, and Subbarao Bondada. "Early Growth Response Genes Regulate B Cell Development, Proliferation, and Immune Response." Journal of Immunology 181, no. 7 (September 18, 2008): 4590–602. http://dx.doi.org/10.4049/jimmunol.181.7.4590.
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SONG, RAN, Igor Dozmorov, Chaoying Liang, Bo Zhang, Benjamin wakeland, carlos Arana, Kasthuribai Viswanathan, Linley Riediger, and Edward Wakeland. "Population diversity in transcriptional responses of macrophages to TLR7/8 signaling (IRM12P.654)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 133.13. http://dx.doi.org/10.4049/jimmunol.194.supp.133.13.
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Abstract The Toll-like receptors (TLR) of the innate immune system play a key role in the recognition of pathogens and the initiation of a robust innate immune response. Although an innate immune response is essential for resistance to pathogen infection, the magnitude and qualities of innate immune responses are quite variable in the human population. Here we performed transcriptome sequencing of monocyte-derived macrophages generated from 78 healthy individuals, including 10 replicates from repeat donors, to profile gene expression patterns in responses to TLR7/8 signaling. Extensive qualitative and quantitative diversity was apparent in the response of individuals in this panel. Cluster analysis discriminated nine distinct clusters of genes expressed in response to the TLR7/8 agonist (R848) with correlated expression variations within this panel. Interestingly, the induction of cytokine and chemokine transcription varied among donors and majority of these genes have very reproducible variability of their expression in 10 replicates. In addition, it was shown that donors with high expression of cytokine and chemokine genes after R848 stimulation were also high responder to Respiratory syncytial virus infection. Thus, there are the variations in gene expression among individuals with TLR7/8 stimulation, indicating that genetic polymorphisms in “master” regulators may correlate expression patterns of multiple genes during innate responses.
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Hewavisenti, Rehana V., Katrina M. Morris, Denis O’Meally, Yuanyuan Cheng, Anthony T. Papenfuss, and Katherine Belov. "The identification of immune genes in the milk transcriptome of the Tasmanian devil (Sarcophilus harrisii)." PeerJ 4 (January 12, 2016): e1569. http://dx.doi.org/10.7717/peerj.1569.
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Tasmanian devil (Sarcophilus harrisii) pouch young, like other marsupials, are born underdeveloped and immunologically naïve, and are unable to mount an adaptive immune response. The mother’s milk provides nutrients for growth and development as well as providing passive immunity. To better understand immune response in this endangered species, we set out to characterise the genes involved in passive immunity by sequencing and annotating the transcriptome of a devil milk sample collected during mid-lactation. At mid-lactation we expect the young to have heightened immune responses, as they have emerged from the pouch, encountering new pathogens. A total of 233,660 transcripts were identified, including approximately 17,827 unique protein-coding genes and 846 immune genes. The most highly expressed transcripts were dominated by milk protein genes such as those encoding early lactation protein, late lactation proteins,α-lactalbumin,α-casein andβ-casein. There were numerous highly expressed immune genes including lysozyme, whey acidic protein, ferritin and major histocompatibility complex I and II. Genes encoding immunoglobulins, antimicrobial peptides, chemokines and immune cell receptors were also identified. The array of immune genes identified in this study reflects the importance of the milk in providing immune protection to Tasmanian devil young and provides the first insight into Tasmanian devil milk.
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Petit, Marine J., Matthew W. Kenaston, Oanh H. Pham, Ariana A. Nagainis, Adam T. Fishburn, and Priya S. Shah. "Nuclear dengue virus NS5 antagonizes expression of PAF1-dependent immune response genes." PLOS Pathogens 17, no. 11 (November 19, 2021): e1010100. http://dx.doi.org/10.1371/journal.ppat.1010100.
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Dengue virus (DENV) disruption of the innate immune response is critical to establish infection. DENV non-structural protein 5 (NS5) plays a central role in this disruption, such as antagonism of STAT2. We recently found that DENV serotype 2 (DENV2) NS5 interacts with Polymerase associated factor 1 complex (PAF1C). The primary members of PAF1C are PAF1, LEO1, CTR9, and CDC73. This nuclear complex is an emerging player in the immune response. It promotes the expression of many genes, including genes related to the antiviral, antimicrobial and inflammatory responses, through close association with the chromatin of these genes. Our previous work demonstrated that NS5 antagonizes PAF1C recruitment to immune response genes. However, it remains unknown if NS5 antagonism of PAF1C is complementary to its antagonism of STAT2. Here, we show that knockout of PAF1 enhances DENV2 infectious virion production. By comparing gene expression profiles in PAF1 and STAT2 knockout cells, we find that PAF1 is necessary to express immune response genes that are STAT2-independent. Finally, we mapped the viral determinants for the NS5-PAF1C protein interaction. We found that NS5 nuclear localization and the C-terminal region of the methyltransferase domain are required for its interaction with PAF1C. Mutation of these regions rescued the expression of PAF1-dependent immune response genes that are antagonized by NS5. In sum, our results support a role for PAF1C in restricting DENV2 replication that NS5 antagonizes through its protein interaction with PAF1C.
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Starr, Izzy, Kristina Seiffert-Sinha, Animesh A. Sinha, and Omer Gokcumen. "Evolutionary context of psoriatic immune skin response." Evolution, Medicine, and Public Health 9, no. 1 (January 1, 2021): 474–86. http://dx.doi.org/10.1093/emph/eoab042.
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Abstract The skin is vital for protecting the body and perceiving external stimuli in the environment. Ability to adapt between environments is in part based on skin phenotypic plasticity, indicating evolved homeostasis between skin and environment. This homeostasis reflects the greater relationship between the body and the environment, and disruptions in this balance may lead to accumulation of susceptibility factors for autoimmune conditions like psoriasis. In this study, we examined the relationship between rapid, lineage-specific evolution of human skin and formation of psoriatic skin responses at the transcriptome level. We collected skin tissue biopsies from individuals with psoriasis and compared gene expression in psoriatic plaques to non-plaque psoriatic skin. We then compared these data with non-psoriatic skin transcriptome data from multiple primate species. We found 67 genes showing human-specific skin expression that are also differentially regulated in psoriatic skin; these genes are significantly enriched for skin barrier function, immunity and neuronal development. We identified six gene clusters with differential expression in the context of human evolution and psoriasis, suggesting underlying regulatory mechanisms in these loci. Human and psoriasis-specific enrichment of neuroimmune genes shows the importance of the ongoing evolved homeostatic relationship between skin and external environment. These results have implications for both evolutionary medicine and public health, using transcriptomic data to acknowledge the importance of an individual’s surroundings on their overall health.
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Waring, Ashley L., Joshua Hill, Brooke M. Allen, Nicholas M. Bretz, Nguyen Le, Pooja Kr, Dakota Fuss, and Nathan T. Mortimer. "Meta-Analysis of Immune Induced Gene Expression Changes in Diverse Drosophila melanogaster Innate Immune Responses." Insects 13, no. 5 (May 23, 2022): 490. http://dx.doi.org/10.3390/insects13050490.
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Organisms are commonly infected by a diverse array of pathogens and mount functionally distinct responses to each of these varied immune challenges. Host immune responses are characterized by the induction of gene expression, however, the extent to which expression changes are shared among responses to distinct pathogens is largely unknown. To examine this, we performed meta-analysis of gene expression data collected from Drosophila melanogaster following infection with a wide array of pathogens. We identified 62 genes that are significantly induced by infection. While many of these infection-induced genes encode known immune response factors, we also identified 21 genes that have not been previously associated with host immunity. Examination of the upstream flanking sequences of the infection-induced genes lead to the identification of two conserved enhancer sites. These sites correspond to conserved binding sites for GATA and nuclear factor κB (NFκB) family transcription factors and are associated with higher levels of transcript induction. We further identified 31 genes with predicted functions in metabolism and organismal development that are significantly downregulated following infection by diverse pathogens. Our study identifies conserved gene expression changes in Drosophila melanogaster following infection with varied pathogens, and transcription factor families that may regulate this immune induction.
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Khunger, Arjun, Erin Piazza, Sarah Warren, Thomas H. Smith, Xing Ren, Andrew White, Nathan Elliott, et al. "CTLA-4 blockade and interferon-α induce proinflammatory transcriptional changes in the tumor immune landscape that correlate with pathologic response in melanoma." PLOS ONE 16, no. 1 (January 11, 2021): e0245287. http://dx.doi.org/10.1371/journal.pone.0245287.
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Patients with locally/regionally advanced melanoma were treated with neoadjuvant combination immunotherapy with high-dose interferon α-2b (HDI) and ipilimumab in a phase I clinical trial. Tumor specimens were obtained prior to the initiation of neoadjuvant therapy, at the time of surgery and progression if available. In this study, gene expression profiles of tumor specimens (N = 27) were investigated using the NanoString nCounter® platform to evaluate associations with clinical outcomes (pathologic response, radiologic response, relapse-free survival (RFS), and overall survival (OS)) and define biomarkers associated with tumor response. The Tumor Inflammation Signature (TIS), an 18-gene signature that enriches for response to Programmed cell death protein 1 (PD-1) checkpoint blockade, was also evaluated for association with clinical response and survival. It was observed that neoadjuvant ipilimumab-HDI therapy demonstrated an upregulation of immune-related genes, chemokines, and transcription regulator genes involved in immune cell activation, function, or cell proliferation. Importantly, increased expression of baseline pro-inflammatory genes CCL19, CD3D, CD8A, CD22, LY9, IL12RB1, C1S, C7, AMICA1, TIAM1, TIGIT, THY1 was associated with longer OS (p < 0.05). In addition, multiple genes that encode a component or a regulator of the extracellular matrix such as MMP2 and COL1A2 were identified post-treatment as being associated with longer RFS and OS. In all baseline tissues, high TIS scores were associated with longer OS (p = 0.0166). Also, downregulated expression of cell proliferation-related genes such as CUL1, CCND1 and AAMP at baseline was associated with pathological and radiological response (unadjusted p < 0.01). In conclusion, we identified numerous genes that play roles in multiple biological pathways involved in immune activation, immune suppression and cell proliferation correlating with pathological/radiological responses following neoadjuvant immunotherapy highlighting the complexity of immune responses modulated by immunotherapy. Our observations suggest that TIS may be a useful biomarker for predicting survival outcomes with combination immunotherapy.
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Stear, Michael, Sarah Preston, David Piedrafita, and Katarzyna Donskow-Łysoniewska. "The Immune Response to Nematode Infection." International Journal of Molecular Sciences 24, no. 3 (January 23, 2023): 2283. http://dx.doi.org/10.3390/ijms24032283.
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Nematode infection is a major threat to the health of humans, domestic animals and wildlife. Nematodes vary in their effect on the host and in the mechanisms underlying immunity but the general features are becoming clear. There is considerable variation among individuals in resistance to infection and much of this variation is due to genetic variation in the immune response. The major histocompatibility complex has a strong influence on resistance to infection but other genes are collectively more important. Resistant individuals produce more IgA, eosinophils, IgE and mast cells than susceptible individuals and this is a consequence of stronger type 2 (Th2) immune responses. A variety of factors promote Th2 responses including genetic background, diet, molecules produced by the parasite and the location of the infection. A variety of cells and molecules including proteins, glycolipids and RNA act in concert to promote responses and to regulate the response. Nematodes themselves also modulate the host response and over 20 parasite-derived immunomodulatory molecules have been identified. Different species of nematodes modulate the immune response in different ways and probably use multiple molecules. The reasons for this are unclear and the interactions among immunomodulators have still to be investigated.
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Collins, Natalie, Jernej Godec, Lihua Zou, Martin C. Mihm, Gad Getz, and W. Nicholas Haining. "Transcriptional Hallmarks Of Tumor Infiltrating Lymphocyte Responses To Melanoma." Blood 122, no. 21 (November 15, 2013): 3491. http://dx.doi.org/10.1182/blood.v122.21.3491.3491.
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Abstract Tumor-infiltrating lymphocytes (TIL) are found in a subset of melanomas. Patients with pronounced TIL responses have an excellent prognosis, suggesting that for those patients, the infiltrating immune cells are part of an effective adaptive and/or innate response to cancer. However, the molecular features of brisk TIL infiltrates have not been analyzed in situ. Moreover, it is not clear whether the features of the immune response to melanoma are shared by other tumors. Here, we used histological grading of TIL infiltrates in melanoma samples from The Cancer Genome Atlas combined with analysis of immune signatures in transcriptional profiles from the same tumors to characterize the molecular features of the immune response to melanoma. To categorize the histological grade of immune infiltrate, we reviewed digital images of 156 melanoma samples, and assigned a TIL grade (0 - 3) based on established criteria. We found that the distribution of TIL grades in our dataset was consistent with previously published analyses. We first tested whether tumors with brisk infiltrate (TIL Grade 2 or 3) showed enrichment of immune signatures relative to those with non-brisk infiltrates (TIL Grade 0 or 1) using gene-set enrichment analysis (GSEA) with a collection of ∼2000 immune-related gene-sets manually curated from published studies of adaptive and innate immunity. We found that 493 immune signatures enriched in brisk tumors (FDR<0.25), while none enriched in non-brisk tumors, suggesting that the histological TIL grade was strongly associated with transcriptional features of an immune response. Gene-sets that enriched in tumors with brisk infiltrates included those derived from CD4 and CD8 T cells (evidenced by increased expression of T cell lineage-specific genes such as CD3G, ZAP70, CD28, TBX21, PRDM1, GZMB, PRF1); those related to monocytes (CD14); as well as Type I interferon response genes (OAS1, IFI44). Surprisingly we did not find enrichment of gene-sets related to CD8 T cell exhaustion. Instead, we found highly significant enrichment of effector CD8 T cell gene-sets that featured effector cytokines, such as IFNG and TNF, and cytokine receptors such as IL-15R and IL-2RB, genes that which are normally decreased in expression in exhausted T cells. This suggests that the transcriptional profile of brisk immune infiltrates in melanoma includes features of highly functional CD8 effector T cell responses and lacks transcriptional features of exhaustion. We next tested whether the signatures of immune response to melanoma were enriched in other tumors. We identified a core set of “TIL hallmark genes” comprised of GSEA leading-edge genes from multiple gene-sets enriched in brisk vs. non-brisk melanoma samples. We then grouped the gene expression profiles of other tumor histologies according to their expression of TIL hallmark genes using single-sample GSEA. In thyroid cancer, for example, we found that the enrichment of melanoma TIL hallmark genes was strongly correlated with the presence of lymphocyte infiltrates, suggesting that there are common features of the immune response to cancer in different tumor types. Our results show that integrated analysis of histology and gene expression profiles from melanoma samples can identify the molecular features of the TIL response. We find evidence for signatures of effective CD8 T cell responses in brisk infiltrate melanomas that are shared by other tumor types. These TIL hallmark genes may help identify molecular subsets of immunogenic tumors, providing novel outcome predictors, and opportunities to stratify immunotherapeutic treatment options. More broadly, this approach can help deconvolve tumor/host gene expression profiles and better characterize the human immune response to cancer. Disclosures: No relevant conflicts of interest to declare.
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Dai, Lingli, Zaixia Liu, Lili Guo, Yuan Chai, Yanda Yang, Yu Wang, Yanfen Ma, Caixia Shi, and Wenguang Zhang. "Multi-Tissue Transcriptome Study of Innate Immune Gene Expression Profiling Reveals Negative Energy Balance Altered the Defense and Promoted System Inflammation of Dairy Cows." Veterinary Sciences 10, no. 2 (February 1, 2023): 107. http://dx.doi.org/10.3390/vetsci10020107.
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Negative energy balance (NEB) during the perinatal period leads to metabolic and immunological disorders in dairy cows, resulting in systemic responses and inflammation. The innate immune system is crucial for the host’s protection and inflammatory response. However, systematic research is still lacking on how NEB affects the innate immune system to alter the ’host defense capability and inflammatory response. In this investigation, raw transcriptome data of adipose, blood, endometrial, hypothalamus, and liver tissues were downloaded from a public database, cleaned, aligned, quantified, and batch-corrected. The innate immune gene list was retrieved from innateDB, followed by the expression matrix of innate immune genes in various tissues for differential expression analysis, principle component analysis (PCA), and gene set enrichment analysis (GSEA). Under the effect of NEB, adipose tissue had the most differentially expressed genes, which were predominantly up-regulated, whereas blood GSEA had the most enriched biological processes, which were predominantly down-regulated. The gene sets shared by different tissues, which are predominantly involved in biological processes associated with defense responses and inflammation, were dramatically down-regulated in endometrial tissues and highly up-regulated in other tissues. Under the impact of NEB, LBP, PTX3, S100A12, and LCN2 play essential roles in metabolism and immunological control. In conclusion, NEB can downregulate the defensive response of innate immune genes in endometrial, upregulate the immune and inflammatory response of other tissues, activate the host defense response, and increase the systemic inflammatory response. The analysis of the effects of NEB on innate immune genes from the multiple tissues analysis provides new insights into the crosstalk between metabolism and immunity and also provides potential molecular targets for disease diagnosis and disease resistance breeding in dairy cows.
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Chandler, Luke M., Michael Rodriguez, and Keith P. Choe. "RNAi screening for modulators of an osmo-sensitive gene response to extracellular matrix damage reveals negative feedback and interactions with translation inhibition." PLOS ONE 18, no. 5 (May 8, 2023): e0285328. http://dx.doi.org/10.1371/journal.pone.0285328.
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In epidermal tissues, extracellular matrices (ECMs) function as barriers between the organism and environment. Despite being at the interface with the environment, little is known about the role of animal barrier ECMs in sensing stress and communicating with cytoprotective gene pathways in neighboring cells. We and others have identified a putative damage sensor in the C. elegans cuticle that regulates osmotic, detoxification, and innate immune response genes. This pathway is associated with circumferential collagen bands called annular furrows; mutation or loss of furrow collagens causes constitutive activation of osmotic, detoxification, and innate immune response genes. Here, we performed a genome-wide RNAi screen for modulators of osmotic stress response gene gpdh-1 in a furrow collagen mutant strain. RNAi of six genes identified in this screen were tested under other conditions and for effects on other stress responses. The functions of these genes suggest negative feedback within osmolyte accumulation pathways and interactions with ATP homeostasis and protein synthesis. Loss of these gpdh-1 modulators had distinct effects on canonical detoxification and innate immune response genes.
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Zhao, Xiuxin, Hanpeng Luo, Haibo Lu, Longgang Ma, Yanqin Li, Jinhuan Dou, Junxing Zhang, Yun Ma, Jianbin Li, and Yachun Wang. "RNA-Seq Analysis of Peripheral Whole Blood from Dairy Bulls with High and Low Antibody-Mediated Immune Responses—A Preliminary Study." Animals 13, no. 13 (July 5, 2023): 2208. http://dx.doi.org/10.3390/ani13132208.
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Enhancing the immune response through breeding is regarded as an effective strategy for improving animal health, as dairy cattle identified as high immune responders are reported to have a decreased prevalence of economically significant diseases. The identification of differentially expressed genes (DEGs) associated with immune responses might be an effective tool for breeding healthy dairy cattle. In this study, antibody-mediated immune responses (AMIRs) were induced by the immunization of hen egg white lysozyme (HEWL) in six Chinese Holstein dairy bulls divided into high- and low-AMIR groups based on their HEWL antibody level. Then, RNA-seq was applied to explore the transcriptome of peripheral whole blood between the two comparison groups. As a result, several major upregulated and downregulated genes were identified and attributed to the regulation of locomotion, tissue development, immune response, and detoxification. In addition, the result of the KEGG pathway analysis revealed that most DEGs were enriched in pathways related to disease, inflammation, and immune response, including antigen processing and presentation, Staphylococcus aureus infection, intestinal immune network for IgA production, cytokine–cytokine receptor interaction, and complement and coagulation cascades. Moreover, six genes (BOLA-DQA5, C5, CXCL2, HBA, LTF, and COL1A1) were validated using RT-qPCR, which may provide information for genomic selection in breeding programs. These results broaden the knowledge of the immune response mechanism in dairy bulls, which has strong implications for breeding cattle with an enhanced AMIR.
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Kang, Soo-Ji, Ji-Su Jun, and Kwang-Won Hong. "Transcriptome Analysis Reveals Immunomodulatory Effect of Spore-Displayed p75 on Human Intestinal Epithelial Caco-2 Cells." International Journal of Molecular Sciences 23, no. 23 (November 22, 2022): 14519. http://dx.doi.org/10.3390/ijms232314519.
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Lacticaseibacillus rhamnosus GG (LGG) can promote intestinal health by modulating the immune responses of the gastrointestinal tract. However, knowledge about the immunomodulatory action of LGG-derived soluble factors is limited. In our previous study, we have displayed LGG-derived p75 protein on the spore surface of Bacillus subtilis. The objective of this study was to determine the effect of spore-displayed p75 (CotG-p75) on immune system by investigating transcriptional response of Caco-2 cells stimulated by CotG-p75 through RNA-sequencing (RNA-seq). RNA-seq results showed that CotG-p75 mainly stimulated genes involved in biological processes, such as response to stimulus, immune regulation, and chemotaxis. KEGG pathway analysis suggested that many genes activated by CotG-p75 were involved in NF-ĸB signaling and chemokine signaling pathways. CotG-p75 increased cytokines and chemokines such as CXCL1, CXCL2, CXCL3, CXCL8, CXCL10, CCL20, CCL22, and IL1B essential for the immune system. In particular, CotG-p75 increased the expression levels of NF-ĸB-related genes such as NFKBIA, TNFAIP3, BIRC3, NFKB2, and RELB involved in immune and inflammatory responses. This study provides genes and pathways involved in immune responses influenced by CotG-p75. These comprehensive transcriptome profiling could be used to elucidate the immunomodulatory action of CotG-p75.
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Ding, Shuai Dominique, Alexandre B. Leitão, Jonathan P. Day, Ramesh Arunkumar, Morgan Phillips, Shuyu Olivia Zhou, and Francis M. Jiggins. "Trans-regulatory changes underpin the evolution of the Drosophila immune response." PLOS Genetics 18, no. 11 (November 7, 2022): e1010453. http://dx.doi.org/10.1371/journal.pgen.1010453.
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When an animal is infected, the expression of a large suite of genes is changed, resulting in an immune response that can defend the host. Despite much evidence that the sequence of proteins in the immune system can evolve rapidly, the evolution of gene expression is comparatively poorly understood. We therefore investigated the transcriptional response to parasitoid wasp infection in Drosophila simulans and D. sechellia. Although these species are closely related, there has been a large scale divergence in the expression of immune-responsive genes in their two main immune tissues, the fat body and hemocytes. Many genes, including those encoding molecules that directly kill pathogens, have cis regulatory changes, frequently resulting in large differences in their expression in the two species. However, these changes in cis regulation overwhelmingly affected gene expression in immune-challenged and uninfected animals alike. Divergence in the response to infection was controlled in trans. We argue that altering trans-regulatory factors, such as signalling pathways or immune modulators, may allow natural selection to alter the expression of large numbers of immune-responsive genes in a coordinated fashion.
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Li, Q., J. Tang, K. Chao, and X. Gao. "P1195 Identification of immune cell infiltration and potential candidate biomarker in anti-IL 12/23 treated Crohn’s disease patients by integrated bioinformatics analysis and machine learning." Journal of Crohn's and Colitis 18, Supplement_1 (January 1, 2024): i2129—i2130. http://dx.doi.org/10.1093/ecco-jcc/jjad212.1325.
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Abstract Background Variations existed in patients' responses to ustekinumab (UST) treatment in Crohn's disease (CD), but the underlying cause remains unknown1. Our objective was to investigate the involvement of immune cells and identify potential biomarkers that linked to the response to IL 12/23 inhibitors in patients with CD. Methods The analysis utilized the GSE207022 dataset, which consisted of 54 non-responders and 9 responders to UST in CD cohort (Table 1). Initially, differentially expressed genes (DEGs) were identified. Subsequently, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were peformed. LASSO regression was used to further screen the most powerful hub genes2. ROC curve analysis was employed to evaluate the predictive performances of these genes. CIBERSORT was used to estimate the proportion of immune cell types. These significantly altered genes were further subjected to clustering analysis into immune cell-related infiltration. To validate the reliability of the candidates, patients prescribed with UST as the first line biologics in our center were included as an independent dataset. Results A total of 99 DEGs were obtained from the integrated dataset. Analyses of GO and KEGG revealed a significant enrichment of immune response pathways in CD patients. We identified nine hub genes (SOCS3, CD55, KDM5D, IGFBP5, LCN2, SLC15A1, XPNPEP2, HLA-DQA2, and HMGCS2) that were primarily associated with the response versus non-response patients. These nine genes accurately predicted treatment response with an area under the curve (AUC) of 0.96. Non-response individuals exhibited a relatively high Th1 cell polarization. Both LCN2 and KDM5D genes showed positive correlations with Th1 cells and the Th1/Th2 ratio. Furthermore, we validated LCN2 and KDM5D genes as effective predictive markers using independent validation datasets (Figure 1). Conclusion Th1 cell polarization was an important cause of non-response to IL-12/23 agents in CD patients, and LCN2 and KDM5D could be used as predictive markers to identify non-response patients effectively. 1. Newman AM, Liu CL, Green MR, et al. Robust enumeration of cell subsets from tissue expression profiles. Nat Methods. 2015;12(5):453-457. doi:10.1038/nmeth.3337. 2. Feagan BG, Sandborn WJ, Gasink C, et al. Ustekinumab as Induction and Maintenance Therapy for Crohn's Disease. N Engl J Med. 2016;375(20):1946-1960. doi:10.1056/NEJMoa1602773.
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Kim, J. J., V. Ayyavoo, M. L. Bagarazzi, M. A. Chattergoon, K. Dang, B. Wang, J. D. Boyer, and D. B. Weiner. "In vivo engineering of a cellular immune response by coadministration of IL-12 expression vector with a DNA immunogen." Journal of Immunology 158, no. 2 (January 15, 1997): 816–26. http://dx.doi.org/10.4049/jimmunol.158.2.816.
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Abstract Recent studies support the importance of investigating a DNA vaccination approach for the immunologic control of HIV-1. In this regard, it may be important to specifically engineer immune responses in order to improve on first generation vaccine attempts. Especially for HIV, induction of cell-mediated immunity may be an important feature for any candidate vaccine. In an attempt to engineer in vivo the enhancement of cellular immune response and to direct Ag-dependent immune response from Th2 to Th1 type, we investigated the role of codelivery of genes for IL-12 and granulocyte-macrophage-CSF along with DNA vaccine formulations for HIV-1 Ag. We found that codelivery of IL-12 expression cassettes with DNA vaccines for HIV-1 in mice resulted in splenomegaly as well as a shift in the specific immune responses induced. The codelivery of IL-12 genes resulted in the reduction of specific Ab response, while the coinjection of granulocyte-macrophage-CSF genes resulted in the enhancement of specific Ab response. In addition, we observed a significant Ag-specific stimulation of T cells with codelivery of both cytokines. Most importantly, we observed a dramatic increase in specific CTL response from the group coimmunized with the HIV-1 DNA vaccine and IL-12 genes. This work demonstrates the power of DNA delivery in vivo for both the production of a new generation of more effective and targeted vaccines or immunotherapies as well as an analytic tool for the molecular dissection of the mechanisms of immune function.
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Badshah, Yasmin, Maria Shabbir, Khushbukhat Khan, and Hashaam Akhtar. "Expression Profiles of Hepatic Immune Response Genes in HEV Infection." Pathogens 12, no. 3 (March 1, 2023): 392. http://dx.doi.org/10.3390/pathogens12030392.
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Hepatitis E is a liver inflammation caused by infection with the hepatitis E virus (HEV). Every year, there are an estimated 20 million HEV infections worldwide, leading to an estimated 3.3 million symptomatic cases of hepatitis E. HEV viral load has been studied about the disease progression; however, hepatic the host gene expression against HEV infection remains unknown. Methods: We identified the expression profiles of hepatic immune response genes in HEV infections. Fresh blood samples were collected from all the study subjects (130 patients and 124 controls) in 3ml EDTA vacutainers. HEV viral load was determined by a real-time PCR. The total RNA was isolated from the blood using the TRIZOL method. The expression of theCCL2, CCL5, CXCL10, CXCL16, TNF, IFNGR1, and SAMSN1 genes was studied in the blood of 130 HEV patients and 124 controls using a real-time PCR. Results: Gene expression profiles indicate high levels of CCL2, CCL5, CXCL10, CXCL16, TNF, IFNGR1, and SAMSN1 genes that might lead to the recruitment of leukocytes and infected cell apoptosis. Conclusion: Our study demonstrated distinct differences in the expression profiles of host immune response-related genes of HEV infections and provided valuable insight into the potential impact of these genes on disease progression.
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Luo, Jian, Zhiqiang Wang, Fang Tang, and Kai Feng. "Immune Defense Mechanism of Reticulitermes chinensis Snyder (Blattodea: Isoptera) against Serratia marcescens Bizio." Insects 13, no. 3 (February 24, 2022): 226. http://dx.doi.org/10.3390/insects13030226.
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Reticulitermes chinensis Snyder is an important pest species in China. Serratia marcescens Bizio (SM1) is a potent biological bacterium. In our lab, we found that SM1 can kill R. chinensis. To date, the interaction between R. chinensis and SM1 has not been studied. Here, we explored immune responses of R. chinensis against SM1 using transcriptome sequencing. To elucidate immune-related genes, we identified 126,153 unigenes from R. chinensis. In total, 178 immune-related differentially expressed genes (DEGs) were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that many cellular responses were enriched in the top 20 terms. Then, we systematically analyzed several cellular immune pathways involved in the response of R. chinensis to SM1, including phagocytosis, autophagy, and endocytosis pathways. Furthermore, the expression profiles of the cellular immune-related genes were assessed using quantitative reverse-transcription PCR, and the expression levels of the selected genes were upregulated. Further results revealed SM1-mediated activation of humoral immune responses genes, including Toll, IMD, and melanization pathways, which suggested the involvement of humoral immune responses in the defense against SM1. This research elucidated the mechanisms underlying the immune defense of R. chinensis against SM1, providing a solid theoretical basis for exploiting new immune suppressive agents to control R. chinensis. Moreover, this study will facilitate the better control of R. chinensis using SM1.
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Luo, Hao, Gao-Lei Liu, Dan Jian, Dan-Dan Liang, Xue-Mei Li, Li Zhong, Bo Yang, et al. "Neoadjuvant Chemotherapy Improves the Immunosuppressive Microenvironment of Bladder Cancer and Increases the Sensitivity to Immune Checkpoint Blockade." Journal of Immunology Research 2022 (July 21, 2022): 1–21. http://dx.doi.org/10.1155/2022/9962397.
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Although tumor immune microenvironment plays an important role in antitumor therapy, few studies explored the gene signatures associated with the tumor immune microenvironment of bladder cancer after neoadjuvant chemotherapy. We examined and analyzed differentially expressed genes from 9 patients with stage I-III bladder cancer by RNA immune-oncology profiling platform. After neoadjuvant chemotherapy, the expressions of 43 genes in 19 pathways and 10 genes in 5 pathways were upregulated and downregulated, respectively. Neoadjuvant chemotherapy also promoted the expression of genes related to the activation of antitumor immune responses and decreased the expression of genes related to tumor proliferation pathways. In addition, neoadjuvant chemotherapy improved tumor response to immune checkpoint blockade. Furthermore, this study also identified several genes that can be used to predict the efficacy of neoadjuvant chemotherapy and their possible molecular mechanisms. In conclusion, neoadjuvant chemotherapy may promote the activation of antitumor effects, improve the suppressive tumor immune microenvironment, and increase the sensitivity of bladder cancer to immune checkpoint blockade.
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Yan, Jia, Ya jun Huang, Qing yu Huang, Peng Xia Liu, and Chang Shan Wang. "Comprehensive analysis of the correlations of S100B with hypoxia response and immune infiltration in hepatocellular carcinoma." PeerJ 10 (March 29, 2022): e13201. http://dx.doi.org/10.7717/peerj.13201.
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S100B has been found to be dysregulated in many cancers including hepatocellular carcinoma (HCC). However, the functions of S100B and its underlying mechanisms in HCC remain poorly understood, especially in the tumor microenvironment. In this study, functions enrichment analysis indicated that S100B expression was correlated with hypoxia and immune responses. We found that hypoxia could induce S100B expression in an HIF-1α-dependent manner in HepG2 cells. Luciferase reporter and ChIP-qRCR assays demonstrated that HIF-1α regulates S100B transcription by directly binding to hypoxia-response elements (HREs) of the S100B promoter. Functionally, knockdown of S100B reduces hypoxia-induced HepG2 cell invasion and migration. Furthermore, GSVA enrichment results displayed that S100B and its co-expressed genes were positively correlated with EMT pathway in HCC. Additionally, GO/KEGG cluster analysis results indicated that co-expressed genes of S100B were involved in biological processes of immune response and multiple tumor immune-related signaling pathways in HCC. S100B expression was positively correlated with multiple immune cells tumor infiltration and associated with chemokines/chemokine receptors and immune checkpoint genes. Moreover, S100B is predominantly expressed in immune cells, especially NK (Natural Killer) cell. In addition, the hub genes of S100B co-expression and hypoxia response in HepG2 cell were also associated with immune cells infiltration in HCC. Taken together, these findings provide a new insight into the complex networks between hypoxia response and immune cells infiltration in tumor microenvironment of liver cancer. S100B maybe serve as a novel target for future HCC therapies.
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Baglivo, Sara, Fortunato Bianconi, Francesca Romana Tofanetti, Biagio Ricciuti, Lorenza Pistola, Annamaria Siggillino, Maria Sole Reda, et al. "Immune gene expression and bayesian network analysis in advanced non small cell lung cancer (NSCLC) patients treated with immunotherapy." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e20693-e20693. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e20693.
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e20693 Background: Immune checkpoint inhibitors (ICIs) have revoluzionized the therapeutic paradigm for different types of cancer including NSCLC. Clinical benefit, however, is limited to a minority of patients. The only adopted predictive biomarker, PD-L1 IHC testing, suffers from some limitations. A better understanding of biomarkers associated with response to ICIs is needed. Here, we studied immune gene expression profile and association with clinical response to immunotherapy in advanced NSCLC patients (pts) treated with ICI. Methods: A total of 37 Formalin-fixed, paraffin-embedded (FFPE) samples from advanced NSCLCs were analyzed by RNA-Seq using the Oncomine Immuno Response Assay (OIRRA) (ThermoFisher Scientific) to measure the expression level of 395 genes associated with 36 functional groups including checkpoint pathways, lymphocyte regulation and cytokine interactions, using the Ion Chef and Ion Torrent PGM. Gene level differential expression analysis were performed with the Torrent Suite and Transcriptome Analysis Console (TAC) 4.0 Software. Gene network analysis based on Bayesian algorithm was performed by GeneMANIA database querying with the genes selected through mRNA expression analysis. Results: Among 37 FFPE samples only 18 showed more than 300 OIRRA detectable target genes. In this subgroup, gene expression analysis revealed 7 genes (CCR2, CRTAM, FASLG, SELL, TIGIT, TNFRSF4, and TP63) up-regulated and one gene (CXCL8) down-regulated (p-value < 0.05) in ICI-responders compare to ICI-no responders. Bayesian enrichment computational analysis of the eight gene expression signature showed a more complex network which involves other 10 genes (SIRPG, GZMK, XCL2, CD8A, CD2, IFNG, SIT1, TAGAP, PTPRC and GZMH), correlated with different functional groups. Three main immune-pathways were identified (p < 0.01) (T cell activation, leucocyte activation and migration) involving TIGIT, TNFRSF4, CCR2 and CXCL8 genes among the gene expression signature identified. Conclusions: Our results revealed an immune response gene expression signature of 8 genes differentially expressed between ICI and ICI-no responders. Cancer systems biology analysis approach strengthen our findings identifying an immune molecular network and confirm the correlation of the gene expression signature with relevant immune regulatory functions. If validated, our results may have an important role for the development of a robust test to select patients properly and predict immune response to enable precision immunotherapy.
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MANDAL, S., L. CURTIS, M. PIND, L. MURPHY, and P. WATSON. "S100A7 (psoriasin) influences immune response genes in human breast cancer." Experimental Cell Research 313, no. 14 (August 15, 2007): 3016–25. http://dx.doi.org/10.1016/j.yexcr.2007.03.020.
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Wake, Claire T., and Richard A. Flavell. "Multiple mechanisms regulate the expression of murine immune response genes." Cell 42, no. 2 (September 1985): 623–28. http://dx.doi.org/10.1016/0092-8674(85)90119-9.
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Wang, Zhiquan, Olivia M. Depies, Sutapa Sinha, Weiguo Han, Sameer A. Parikh, and Neil E. Kay. "Aberrant Heterochromatin Silences Immune Response Genes in Chronic Lymphocytic Leukemia." Blood 142, Supplement 1 (November 28, 2023): 3258. http://dx.doi.org/10.1182/blood-2023-182898.
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Introduction: Recent studies have shown that clonal B cells derived from patients with chronic lymphocytic leukemia (CLL) have altered histone modification landscapes compared to B cells from healthy controls. We have also shown that the BCR signaling pathway impacts the chromatin landscapes of CLL B cells, implicating the interaction between oncogenic signaling and epigenetic machinery in CLL (Wang et al., Blood Cancer J. 2022; Wang et al., Cancer Res (2023) 83 (7_Supplement): 4725). However, the majority of the chromatin studies in CLL concentrate on the active enhancers associated with oncogene expression; there is a very limited understanding of lost enhancers in CLL: 1) What is the function of lost enhancers; 2) How are these lost enhancers maintained in CLL; 3) Can these lost enhancers be detected at the precursor state of CLL, monoclonal B-cell lymphocytosis (MBL); 4) if this aberrant chromatin signature affected by CLL treatment. Methods: We systematically mapped the genome-wide histone modification profile (histone marks: H3K4me1, H3K4me3, H3K9me3, H3K27ac, H3K27me3, and H3K36me3) in 22 previously untreated CLL samples, 6 high count MBL samples, and peripheral blood B cells from 6 healthy donors by Cleavage Under Targets and Tagmentation (CUT&Tag). We also analyzed B cells from 8 patients before and after one year of continuous Bruton tyrosine kinase inhibitor (BTKi) ibrutinib treatment. The genomic regions with a decrease in both H3K4me1 and H3K27ac enrichment (analyzed by Deseq2, fold change > 1, p < 0.01) were named lost enhancers. We used CRISPR-mediated epigenetic editing to study the role of gained H3K9me3 on EBF1 gene expression. Results: Compared to normal B cells, the lost enhancers (genomic regions defined by decreased enrichment of H3K4me1 and H3K27ac) in CLL B cells showed increased heterochromatin marks (H3K9me3 and H3K27me3) enrichment. Importantly, these enhancers are associated with genes downregulated in CLL and involved in the immune response, indicating the source of epigenetic impact on impaired immunity in CLL. We further found that this aberrant chromatin structure also exits in clonal B cells from the precursor stage of MBL, implicating the importance of epigenetic silencing in CLL evolution. In particular, we found the lost enhancer signature across the gene locus EBF1, an important transcription factor that defines B cell lineage and regulates normal B cell activation. Using CRISPR-mediated epigenetic editing, we demonstrated that the gain of H3K9me3 is sufficient to silence the EBF1 enhancer and its gene expression. Finally, we found that while BTKi ibrutinib treatment partially inhibits the CLL-gained enhancers in some patients, it failed to restore the lost enhancers in CLL B cells. Conclusion: In summary, we have elucidated an epigenetic silencing mechanism that may contribute to the loss of physiological function of normal B cells, which places the clonal B cells at a selection advantage during CLL evolution and increases the risk of serious infections in CLL and MBL ( Fig 1).