A carregar...
Publicação
Inhibition of murine γδ lymphocyte expansion and effector function by regulatory αβ T cells is cell-contact-dependent and sensitive to GITR modulation
| Nome: | Descrição: | Tamanho: | Formato: | |
|---|---|---|---|---|
| 495.28 KB | Adobe PDF |
Orientador(es)
Resumo(s)
γδ T cells are highly cytolytic lymphocytes that produce large amounts of pro-inflammatory cytokines during immune responses to multiple pathogens. Furthermore, their ability to kill tumor cells has fueled the development of γδ-T-cell-based cancer therapies. Thus, the regulation of γδ-T-cell activity is of great biological and clinical relevance. Here, we show that murine CD4+CD25+ αβ T cells, the vast majority of which express the Treg marker, Foxp3, abolish key effector functions of γδ T cells, namely the production of the pro-inflammatory cytokines, IFN-γ and IL-17, cytotoxicity, and lymphocyte proliferation in vitro and in vivo. We further show that suppression is dependent on cellular contact between Treg and γδ T cells, results in the induction of an anergic state in γδ lymphocytes, and can be partially reversed by manipulating glucocorticoid-induced TNF receptor-related protein (GITR) signals. Our data collectively dissect a novel mechanism by which the expansion and pro-inflammatory functions of γδ T cells are regulated.
Descrição
© 2010 WILEY
Palavras-chave
γδ T cells IFN-γ IL-17 Treg T-cell suppression
Contexto Educativo
Citação
Eur. J. Immunol. 2010. 40: 61–70