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Interleukin 17A (IL-17A) is a potent pro-inflammatory cytokine primarily secreted by Th17 cells, as well as other immune cells like gamma-delta T cells and innate lymphoid cells [1, 2]. It serves as a key mediator in the host's defense against extracellular pathogens, particularly bacteria and fungi, by stimulating the production of chemokines, proinflammatory cytokines, and antimicrobial peptides from various cell types [2, 3]. In many autoimmune and chronic inflammatory diseases, IL-17A is overproduced, leading to tissue damage and persistent inflammation [3]. This cytokine is a major therapeutic target in dermatology and rheumatology, with several approved monoclonal antibodies designed to neutralize its activity [4, 5]. While highly effective for treating plaque psoriasis and spondyloarthritides, its inhibition requires careful monitoring due to risks such as increased fungal infections and the potential to trigger or worsen inflammatory bowel disease [5, 6]. Consequently, IL-17A remains a cornerstone of modern biologic therapy for Th17-mediated pathologies [4].
Monoclonal antibodies target and bind to the IL-17A cytokine, preventing it from interacting with its receptor complex (comprising IL-17RA and IL-17RC) on target cells [4, 5]. This blockade inhibits the activation of downstream signaling pathways, such as NF-kappaB and MAPK, thereby reducing the production of inflammatory mediators like IL-6, G-CSF, and various CXCL chemokines [2, 3].
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