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Please join us for PhD Student, Dhruv Patel’s Graduate Student Literature Seminar.
Nearly 4% of world population suffers from autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis (MS), inflammatory bowel disease, allergy, and asthma. Several environmental and genetic factors play a role in these conditions. Certain autoimmune and inflammatory diseases, such as MS, are driven by IL-17 producing CD4+ T cells subset (T helper 17 cells) and thus are exploited for immunotherapies. Transforming growth factor-β and pro-inflammatory cytokines, such as IL-1β, IL-6, IL-17, IL-21, and IL-23, play a central role in generation of Th17 cells. With IL-6, IL-1β and IL-23 cytokine exposure, naïve CD4+ T cells differentiate into pathogenic Th17 cells. Upregulation of let-7 miRNAs protects against experimental autoimmune encephalomyelitis (EAE, animal model of MS) by downregulating proliferation of pathogenic Th17 cells. Let-7 miRNA directly targets inflammatory cytokine receptor IL1r1 and IL23r, which inhibits the positive feedback loop in pathogenic Th17 cells. Th17 cells also increase mitochondrial respiration which results in more cell proliferation. Inhibition of mitochondrial oxidative phosphorylation and ATP synthase removes Th17 pathogenicity in EAE mouse model. This literature review aims to identify genes associated with pathogenicity of Th17 cells and potential therapeutic application for disease treatment.
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