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首页> 外文期刊>Nature immunology >Interleukin 10 acts on regulatory T cells to maintain expression of the transcription factor Foxp3 and suppressive function in mice with colitis.
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Interleukin 10 acts on regulatory T cells to maintain expression of the transcription factor Foxp3 and suppressive function in mice with colitis.

机译:白介素10作用于调节性T细胞,以维持结肠炎小鼠中转录因子Foxp3的表达和抑制功能。

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摘要

Regulatory T cells (T(reg) cells) that express the transcription factor Foxp3 suppress the activity of other cells. Here we show that interleukin 10 (IL-10) produced by CD11b(+) myeloid cells in recombination-activating gene 1-deficient (Rag1(-/-)) recipient mice was needed to prevent the colitis induced by transferred CD4(+)CD45RB(hi) T cells. In Il10(-/-)Rag1(-/-) mice, T(reg) cells failed to maintain Foxp3 expression and regulatory activity. The loss of Foxp3 expression occurred only in recipients with colitis, which indicates that the requirement for IL-10 is manifested in the presence of inflammation. IL-10 receptor-deficient (Il10rb(-/-)) T(reg) cells also failed to maintain Foxp3 expression, which suggested that host IL-10 acted directly on the T(reg) cells. Our data indicate that IL-10 released from myeloid cells acts in a paracrine manner on T(reg) cells to maintain Foxp3 expression.
机译:表达转录因子Foxp3的调节性T细胞(T(reg)细胞)抑制其他细胞的活性。在这里,我们显示需要CD11b(+)髓样细胞在重组激活基因1缺陷(Rag1(-/-))受体小鼠中产生的白介素10(IL-10),以防止转移CD4(+)引起的结肠炎CD45RB(hi)T细胞。在Il10(-/-)Rag1(-/-)小鼠中,T(reg)细胞未能维持Foxp3表达和调节活性。 Foxp3表达的丧失仅发生在患有结肠炎的接受者中,这表明对IL-10的需求在炎症存在时得以体现。 IL-10受体缺陷(Il10rb(-/-))T(reg)细胞也无法维持Foxp3表达,这表明宿主IL-10直接作用于T(reg)细胞。我们的数据表明,从髓样细胞释放的IL-10以旁分泌的方式作用于T(reg)细胞,以维持Foxp3表达。

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