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Interleukin-17A (IL-17A) is a potent pro-inflammatory cytokine primarily produced by Th17 cells, a specialized subset of CD4+ T helper cells (UniProt Q16552). It exists as a disulfide-linked homodimer, referred to as IL-17AA, which signals through a heteromeric receptor complex consisting of IL-17RA and IL-17RC (PubMed: 27110333). IL-17A plays a pivotal role in the immune system by inducing the expression of chemokines, cytokines, and antimicrobial peptides that recruit neutrophils and protect against fungal and bacterial infections (PubMed: 21169545). Pathologically, the overproduction of IL-17A is a central driver in chronic inflammatory conditions, most notably plaque psoriasis, psoriatic arthritis, and axial spondyloarthritis (PubMed: 25114214). Therapeutic strategies targeting the IL-17AA homodimer involve monoclonal antibodies such as secukinumab and ixekizumab, which neutralize the cytokine and prevent receptor activation (FDA: Cosentyx, Taltz). While these therapies are highly effective in clearing skin lesions and reducing joint inflammation, they are associated with specific safety concerns, including an increased risk of mucocutaneous candidiasis and the potential for exacerbating inflammatory bowel disease (PubMed: 29147134).
Neutralization of the IL-17A cytokine to prevent its binding to the IL-17 receptor complex (IL-17RA/IL-17RC), thereby inhibiting downstream inflammatory signaling.
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