Interleukin 10 acts on regulatory T cells to maintain expression of the transcription factor Foxp3 and suppressive function in mice with colitis.
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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表达转录因子Foxp 3的调节性T细胞（Treg细胞）抑制其他细胞的活性。在这里，我们表明，在重组激活基因1缺陷（Rag 1 −/−）受体小鼠中，CD 11b+骨髓细胞产生的白细胞介素10（IL-10）是预防转移的CD 4 + CD 45 RBhi T细胞诱导的结肠炎所必需的。在Il 10 −/− Rag 1 −/−小鼠中，Treg细胞未能维持Foxp 3表达和调节活性。Foxp 3表达的丧失仅发生在患有结肠炎的受者中，这表明对IL-10的需求在炎症的存在下表现出来。IL-10受体缺陷型Treg细胞也不能维持Foxp 3的表达，这表明宿主IL-10直接作用于Treg细胞。我们的数据表明，从骨髓细胞释放的IL-10以旁分泌方式作用于Treg细胞以维持Foxp 3表达。
Regulatory T cells (Treg 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+ CD45RBhi T cells. In Il10 −/− Rag1−/− mice, Treg 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−/−) Treg cells also failed to maintain Foxp3 expression, which suggested that host IL-10 acted directly on the Treg cells. Our data indicate that IL-10 released from myeloid cells acts in a paracrine manner on Treg cells to maintain Foxp3 expression.
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影响因子：
32.4
作者：
Fontenot, JD;Rasmussen, JP;Rudensky, AY
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Rudensky, AY
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15.3
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影响因子：
29.4
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通讯作者：
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作者：
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通讯作者：
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作者：
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通讯作者：
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