Alarmin' immunologists: IL-33 as a putative target for modulating T cell-dependent responses.

Tania Gajardo Carrasco, Rodrigo A. Morales, Francisco Pérez, Claudia Terraza, Luz Yáñez, Mauricio Campos-Mora, Karina Pino-Lagos*

*Autor correspondiente de este trabajo

Resultado de la investigación: Contribución a una revistaArtículo de revisiónrevisión exhaustiva

25 Citas (Scopus)

Resumen

IL-33 is a known member of the IL-1 cytokine superfamily classically named “atypical” due to its diverse functions. The receptor for this cytokine is the ST2 chain (or IL-1RL1), part of the IL-1R family, and the accessory chain IL-1R. ST2 can be found as both soluble and membrane-bound forms, property that explains, at least in part, its wide range of functions. IL-33 has increasingly gained our attention as a potential target to modulate immune responses. At the beginning, it was known as one of the participants during the development of allergic states and other Th2-mediated responses and it is now accepted that IL-33 contributes to Th1-driven pathologies as demonstrated in animal models of experimental autoimmune encephalomyelitis (EAE), collagen-induced arthritis, and trinitrobenzene sulfonic acid-induced experimental colitis, among others. Interestingly, current data are placing IL-33 as a novel regulator of immune tolerance by affecting regulatory T cells (Tregs); although the mechanism is not fully understood, it seems that dendritic cells and myeloid suppressor-derived cells may be cooperating in the generation and/or establishment of IL-33-mediated tolerance. Here, we review the most updated literature on IL-33, its role on T cell biology, and its impact in immune tolerance.
Idioma originalInglés
Número de artículo232
PublicaciónFrontiers in Immunology
Volumen6
N.ºJUN
DOI
EstadoPublicada - 2015

Nota bibliográfica

Publisher Copyright:
© 2015 Gajardo Carrasco, Morales, Pérez, Terraza, Yáñez, Campos-Mora and Pino-Lagos.

Huella

Profundice en los temas de investigación de 'Alarmin' immunologists: IL-33 as a putative target for modulating T cell-dependent responses.'. En conjunto forman una huella única.

Citar esto