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Abstract: 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-?B) 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 (??) T cells, alpha beta (??) 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.
Fuente: Frontiers in Immunology, 2023, 14, 1191782 - (CORRIGENDUM), 2023, 14, 1332177
Editorial: Frontiers Research Foundation
Año de publicación: 2023
Nº de páginas: 14
Tipo de publicación: Artículo de Revista
DOI: 10.3389/fimmu.2023.1191782
ISSN: 1664-3224
Url de la publicación: https://doi.org/10.3389/fimmu.2023.1191782
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NAVARRO-COMPÁN, VICTORIA
PUIG, LULIS
VIDAL, SILVIA
RAMÍREZ, JULIO
LLAMAS-VELASCO, MAR
FERNÁNDEZ-CARBALLIDO, CRISTINA
ALMODÓVAR, RAQUEL
PINTO, JOSÉ ANTONIO
GALÍNEZ-AGUIRREGOIKOA, EVA
ZARCO, PEDRO
JOVEN, BEATRIZ
GRATACÓS, JORDI
JUANOLA, XAVIER
RICARDO BLANCO ALONSO
ARIAS-SANTIAGO, SALVADOR
SANZ SANZ, JESÚS
QUEIRO, RUBÉN
CAÑETE, JUAND D.
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