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|Title: ||Inhibition of murine γδ lymphocyte expansion and effector function by regulatory αβ T cells is cell-contact-dependent and sensitive to GITR modulation|
|Authors: ||Gonçalves-Sousa, Natacha|
Ribot, Julie C.
Barros, Ana de
Correia, Daniel V.
|Keywords: ||γδ T cells|
|Issue Date: ||2010|
|Citation: ||Eur. J. Immunol. 2010. 40: 61–70|
|Abstract: ||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.|
|Description: ||© 2010 WILEY|
|Peer Reviewed: ||yes|
|Appears in Collections:||IMM - Artigos em Revistas Internacionais|
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