Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/17561
Título
Interleukin-17A Serves a Priming Role in Autoimmunity by Recruiting IL-1β-Producing Myeloid Cells that Promote Pathogenic T Cells.
Autor(es)
Fecha de publicación
2020-02-18
Cita
Immunity . 2020;52(2):342-356
Idioma
Inglés
Tipo de documento
journal article
Resumen
Interleukin-17A (IL-17A) is a major mediator of tissue inflammation in many autoimmune diseases. Anti-IL-17A is an effective treatment for psoriasis and is showing promise in clinical trials in multiple sclerosis. In this study, we find that IL-17A-defective mice or mice treated with anti-IL-17A at induction of experimental autoimmune encephalomyelitis (EAE) are resistant to disease and have defective priming of IL-17-secreting γδ T (γδT17) cells and Th17 cells. However, T cells from Il17a-/- mice induce EAE in wild-type mice following in vitro culture with autoantigen, IL-1β, and IL-23. Furthermore, treatment with IL-1β or IL-17A at induction of EAE restores disease in Il17a-/- mice. Importantly, mobilization of IL-1β-producing neutrophils and inflammatory monocytes and activation of γδT17 cells is reduced in Il17a-/- mice. Our findings demonstrate that a key function of IL-17A in central nervous system (CNS) autoimmunity is to recruit IL-1β-secreting myeloid cells that prime pathogenic γδT17 and Th17 cells.
MESH
Animals | Autoantigens | Autoimmunity | Central Nervous System | Encephalomyelitis, Autoimmune, Experimental | Interleukin-17 | Interleukin-1beta | Interleukin-23 | Intraepithelial Lymphocytes | Mice | Mice, Inbred C57BL | Mice, Knockout | Monocytes | Myeloid Cells | Neutrophils | Th17 Cells
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