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T helper cell 17 (Th17) is a distinct subset of CD4+ effector T cells that is defined by the production of its signature cytokines, interleukin-17A (IL-17A), IL-17F, and IL-22 (StatPearls, NBK541082). These cells differentiate from naive T cells under the influence of cytokines like TGF-beta, IL-6, and IL-23, which activate the master transcription factor RORgamma-t (Nature Reviews Immunology, 2017). Biologically, Th17 cells are essential for host defense against extracellular pathogens, such as bacteria and fungi, by recruiting neutrophils and inducing the production of antimicrobial peptides at mucosal surfaces (PubMed, 28418795). However, their dysregulation is a primary driver of chronic inflammatory and autoimmune diseases, including psoriasis, psoriatic arthritis, and ankylosing spondylitis (JCI, 121734). In these conditions, Th17 cells contribute to tissue damage and persistent inflammation through the continuous secretion of pro-inflammatory mediators. Therapeutic strategies targeting the Th17 axis have revolutionized the treatment of these disorders, utilizing monoclonal antibodies like secukinumab and ixekizumab to neutralize IL-17A, or guselkumab to target the IL-23/Th17 maintenance pathway (Lancet Rheumatology, 2021). While highly effective, these interventions carry a specific risk of mucocutaneous candidiasis, reflecting the cell's fundamental role in fungal immunity.
Inhibition of the Th17 axis via neutralization of IL-17A, IL-17F, or IL-23, or by blocking the IL-17 receptor (IL-17RA).
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