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T helper 17 (Th17) cells are a specialized subset of CD4+ T lymphocytes characterized by their production of pro-inflammatory cytokines, including IL-17A, IL-17F, and IL-22 [PubMed: 17291286]. Their development is governed by the master transcription factor RORγt and is induced by a specific cytokine environment containing TGF-β, IL-6, and IL-23 [PubMed: 28435039]. While Th17 cells are critical for mucosal immunity and defense against extracellular bacteria and fungi, their dysregulation is a primary driver in the pathogenesis of chronic inflammatory and autoimmune diseases such as psoriasis, rheumatoid arthritis, and multiple sclerosis [PubMed: 30107052]. In drug discovery, the Th17 pathway is targeted using monoclonal antibodies like secukinumab or ixekizumab to neutralize effector cytokines, or agents like guselkumab that block the IL-23 survival signal [PubMed: 28247072]. Although highly effective in treating inflammation, inhibiting Th17 function compromises mucosal barriers, leading to a notable risk of fungal infections like Candidiasis [PubMed: 26364239]. Circulating Th17 cell levels are frequently monitored as biomarkers for disease activity and therapeutic response in clinical settings.
Therapeutic agents modulate this cell population by either neutralizing the effector cytokines they produce (such as IL-17A or IL-17F) or by blocking upstream cytokines like IL-23 that are required for their differentiation, survival, and expansion [PubMed: 28247072].
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