Th17 cell differentiation
Core of basic research: Clarifies the molecular mechanism by which naive CD4+ T cells differentiate into Th17 cells under specific cytokine combinations (IL-6 + TGF-β). Th17 cells participate in inflammation and autoimmune diseases by secreting IL-17A/F. IL-6 activates STAT3, and TGF-β activates Smad2/3; both synergistically induce expression of the core transcription factor RORγt, which initiates transcription of genes such as IL-17A/F, IL-21, and IL-22. IL-23 maintains Th17 cell survival and functional stability by activating STAT3. Th17 cells antagonize Th1 and Th2 cells to co-regulate immune balance. Research focuses on the specific regulation of differentiation by cytokine combinations, interactions between RORγt and other transcription factors (e.g., Foxp3), Th17 cell plasticity (e.g., conversion to IFN-γ+ cells in inflammatory microenvironments), and excessive Th17 cell proliferation mechanisms in autoimmune diseases (e.g., multiple sclerosis, psoriasis).
Core key proteins: Naive CD4+ T cells, IL-6, TGF-β, STAT3, RORγt (core transcription factor), IL-17A/F, IL-21/IL-22 (signature Th17 cytokines), IL-23/IL-23R (maintains Th17 function), Foxp3 (antagonizes RORγt), IL-1β (enhances differentiation), CCR6 (Th17 cell chemokine receptor).
Core key proteins: Naive CD4+ T cells, IL-6, TGF-β, STAT3, RORγt (core transcription factor), IL-17A/F, IL-21/IL-22 (signature Th17 cytokines), IL-23/IL-23R (maintains Th17 function), Foxp3 (antagonizes RORγt), IL-1β (enhances differentiation), CCR6 (Th17 cell chemokine receptor).
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