"T-bet"-ing on autoimmunity variants
نویسندگان
چکیده
1 Department of Microbiology and Immunology, University of California, San Francisco, California, United States of America, 2 Diabetes Center, University of California, San Francisco, California, United States of America, 3 Innovative Genomics Institute, University of California, Berkeley, California, United States of America, 4 Biomedical Sciences Graduate Program, University of California, San Francisco, California, United States of America, 5 Department of Medicine, University of California, San Francisco, California, United States of America, 6 UCSF Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, California, United States of America, 7 Chan Zuckerberg Biohub, San Francisco, California, United States of America
منابع مشابه
Genetic variants alter T-bet binding and gene expression in mucosal inflammatory disease
The polarization of CD4+ T cells into distinct T helper cell lineages is essential for protective immunity against infection, but aberrant T cell polarization can cause autoimmunity. The transcription factor T-bet (TBX21) specifies the Th1 lineage and represses alternative T cell fates. Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) that may be causative ...
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Gene association studies are less appealing in cancer compared to autoimmune diseases. Complexity, heterogeneity, variation in histological types, age at onset, short survival, and acute versus chronic conditions are cancer related factors which are different from an organ specific autoimmune disease, such as Grave’s disease, on which a large body of multicentre data is accumulated. For years t...
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T cell receptor (TCR) affinity is a critical factor of Treg lineage commitment, but whether self-reactivity is a determining factor in peripheral Treg function remains unknown. Here, we report that a high degree of self-reactivity is crucial for tissue-specific Treg function in autoimmunity. Based on high expression of CD5, we identified a subset of self-reactive Tregs expressing elevated level...
متن کاملCutting edge: the pathogenicity of IFN-γ-producing Th17 cells is independent of T-bet.
During the development of experimental autoimmune encephalomyelitis (EAE), the proportion of pathogenic and myelin-specific cells within CNS-infiltrating cytokine-producing Th cells is unknown. Using an IL-17A/IFN-γ double reporter mouse and I-A(b)/myelin oligodendrocyte glycoprotein 38-49 tetramer, we show in this study that IL-17(+)IFN-γ(+) Th cells, which are expanded in the CNS during EAE, ...
متن کاملT-bet negatively regulates autoimmune myocarditis by suppressing local production of interleukin 17
Experimental autoimmune myocarditis (EAM) appears after infectious heart disease, the most common cause of dilated cardiomyopathy in humans. Here we report that mice lacking T-bet, a T-box transcription factor required for T helper (Th)1 cell differentiation and interferon (IFN)-gamma production, develop severe autoimmune heart disease compared to T-bet+/+ control mice. Experiments in T-bet-/- ...
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