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题目:: γδ T cells enhance autoimmunity by restraining regulatory T cell responses via an interleukin-23-dependent mechanism.
作者:: Petermann(Franziska),Rothhammer(Veit),Claussen(Malte C),Haas(Jan D),Blanco(Lorena Riol),Heink(Sylvia),Prinz(Immo),Hemmer(Bernhard),Kuchroo(Vijay K),Oukka(Mohamed),Korn(Thomas)
状态:: 发布时间2010-09-27 , 更新时间 2016-11-22
期刊:: Immunity
摘要:: Mice that lack interleukin-23 (IL-23) are resistant to T cell-mediated autoimmunity. Although IL-23 is a maturation factor for T helper 17 (Th17) cells, a subset of γδ T cells expresses the IL-23 receptor (IL-23R) constitutively. Using IL-23R reporter mice, we showed that γδ T cells were the first cells to respond to IL-23 during experimental autoimmune encephalomyelitis (EAE). Although γδ T cells produced Th17 cell-associated cytokines in response to IL-23, their major function was to prevent the development of regulatory T (Treg) cell responses. IL-23-activated γδ T cells rendered αβ effector T cells refractory to the suppressive activity of Treg cells and also prevented the conversion of conventional T cells into Foxp3(+) Treg cells in vivo. Thus, IL-23, which by itself has no direct effect on Treg cells, is able to disarm Treg cell responses and promote antigen-specific effector T cell responses via activating γδ T cells.
语言:: eng
DOI:

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