The IL-17 family includes cytokines involved in both acute and chronic inflammatory responses. Since IL-17A was identified in 1993, five other members (IL-17B to IL-17F) have been discovered, with IL-17A and IL-17F being the most closely related. These cytokines generally function as homodimers, except for IL-17A and IL-17F, which can form heterodimers. Their signaling requires a receptor complex of IL-17RA and IL-17RC, activating inflammation via NF-κB and MAPK pathways. IL-17A plays a key role in autoimmune and chronic inflammatory diseases, with therapies targeting IL-17 effective in conditions like psoriasis, psoriatic arthritis, and ankylosing spondylitis (axSpA). Both IL-17A and IL-17F are produced by various immune cells, including Th17 cells, stimulating inflammatory mediators such as TNF, IL-1, and IL-6.

Targeting IL-17A and IL-17F has shown efficacy in several immune-mediated inflammatory diseases (IMIDs), though responses vary. Blocking IL-17A is effective for psoriasis, psoriatic arthritis, and axSpA, but less so in inflammatory bowel disease (IBD). While IL-17F is less potent than IL-17A, it still contributes to inflammation, and dual blockade of both cytokines has proven more effective in suppressing inflammatory mediators. Bimekizumab, a dual IL-17A/F inhibitor, has shown superior efficacy in treating psoriasis and psoriatic arthritis, with benefits in axSpA. Other therapies, like sonelokimab, are also under investigation. Dual cytokine inhibition may offer more comprehensive disease control than targeting IL-17A alone.

Reference: Sánchez-Rodríguez G, Puig L. Pathogenic Role of IL-17 and Therapeutic Targeting of IL-17F in Psoriatic Arthritis and Spondyloarthropathies. Int J Mol Sci. 2023 Jun 18;24(12):10305. doi: 10.3390/ijms241210305. PMID: 37373452; PMCID: PMC10299014.