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Interleukin-23 subunit alpha (IL-23A), also known as p19, is a cytokine that forms the functional IL-23 protein when covalently linked to the IL-12p40 subunit (UniProt: Q9NPF7). IL-23 is a key driver of the Th17 immune response, promoting the survival and expansion of Th17 cells which produce pro-inflammatory cytokines like IL-17A, IL-17F, and IL-22 (PubMed: 28127412). This signaling pathway is fundamental to the pathogenesis of various autoimmune and inflammatory disorders, including plaque psoriasis, psoriatic arthritis, and inflammatory bowel diseases like Crohn's disease (StatPearls: NBK560819). Unlike IL-12, which shares the p40 subunit and drives Th1 responses, IL-23 is specifically linked to chronic tissue inflammation (NCBI Gene: 51561). Therapeutic targeting of the IL-23A subunit using monoclonal antibodies such as guselkumab and risankizumab allows for selective inhibition of the IL-23 pathway while sparing IL-12-mediated immunity, offering a refined approach to treating inflammatory conditions (DrugBank: DB11911). These drugs have shown significant clinical efficacy in clearing skin lesions and reducing intestinal inflammation with a manageable safety profile (PubMed: 30509639).
Monoclonal antibody that binds to the p19 subunit of interleukin-23, inhibiting its interaction with the IL-23 receptor complex and preventing the activation of the Th17 inflammatory pathway.
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