The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases

Interleukin-17 family (IL-17s) comprises six structurally related members (IL-17A to IL-17F); sequence homology is highest between IL-17A and IL-17F, displaying certain overlapping functions. In general, IL-17A and IL-17F play important roles in chronic inflammation and autoimmunity, controlling bac...

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Detalles Bibliográficos
Autores: Navarro-Compán, Victoria, Puig Sanz, Lluís|||0000-0001-6083-0952, Vidal, Silvia|||0000-0002-3909-6682, Ramírez, Julio, Llamas-Velasco, Mar|||0000-0002-1187-1341, Fernández-Carballido, Cristina|||0000-0002-0910-4944, Almodóvar, Raquel, Pinto, José Antonio, Galíndez Agirregoikoa, Eva, Zarco, Pedro, Joven Ibáñez, Beatriz, Gratacós, Jordi|||0000-0003-4007-4103, Juanola, Xavier|||0000-0001-5998-6300, Blanco, Ricardo|||0000-0003-2344-2285, Arias-Santiago, Salvador|||0000-0002-4186-1435, Sanz Sanz, Jesús, Queiro, Ruben|||0000-0002-8418-7145, Cañete, Juan D.|||0000-0003-2606-0573
Tipo de recurso: artículo
Fecha de publicación:2023
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:290195
Acceso en línea:https://ddd.uab.cat/record/290195
https://dx.doi.org/urn:doi:10.3389/fimmu.2023.1191782
Access Level:acceso abierto
Palabra clave:IL-17A
IL-17F
IL-23
MAIT cells
Psoriasis
Spondyloarthritis
Th17 cells
γδ T cells
Descripción
Sumario:Interleukin-17 family (IL-17s) comprises six structurally related members (IL-17A to IL-17F); sequence homology is highest between IL-17A and IL-17F, displaying certain overlapping functions. In general, IL-17A and IL-17F play important roles in chronic inflammation and autoimmunity, controlling bacterial and fungal infections, and signaling mainly through activation of the nuclear factor-kappa B (NF-κB) pathway. The role of IL-17A and IL-17F has been established in chronic immune-mediated inflammatory diseases (IMIDs), such as psoriasis (PsO), psoriatic arthritis (PsA), axial spondylarthritis (axSpA), hidradenitis suppurativa (HS), inflammatory bowel disease (IBD), multiple sclerosis (MS), and asthma. CD4 + helper T cells (Th17) activated by IL-23 are well-studied sources of IL-17A and IL-17F. However, other cellular subtypes can also produce IL-17A and IL-17F, including gamma delta (γδ) T cells, alpha beta (αβ) T cells, type 3 innate lymphoid cells (ILC3), natural killer T cells (NKT), or mucosal associated invariant T cells (MAIT). Interestingly, the production of IL-17A and IL-17F by innate and innate-like lymphocytes can take place in an IL-23 independent manner in addition to IL-23 classical pathway. This would explain the limitations of the inhibition of IL-23 in the treatment of patients with certain rheumatic immune-mediated conditions such as axSpA. Despite their coincident functions, IL-17A and IL-17F contribute independently to chronic tissue inflammation having somehow non-redundant roles. Although IL-17A has been more widely studied, both IL-17A and IL-17F are overexpressed in PsO, PsA, axSpA and HS. Therefore, dual inhibition of IL-17A and IL-17F could provide better outcomes than IL-23 or IL-17A blockade.

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