Different populations of CD11b(+) dendritic cells drive Th2 responses in the small intestine and colon.
Different populations of CD11b(+) dendritic cells drive Th2 responses in the small intestine and colon.
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DOI：
10.1038/ncomms15820
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发表时间：
2017-06-09
影响因子：
16.6
通讯作者：
Milling SW
中科院分区：
文献类型：
--
作者：
Mayer JU;Demiri M;Agace WW;MacDonald AS;Svensson-Frej M;Milling SW
辅助性T细胞2（Th 2）应答防御寄生虫。虽然树突状细胞（DC）对于诱导T细胞应答是至关重要的，但是在肠中诱导Th 2细胞的DC亚群是未鉴定的。在这里，我们表明，肠道Th 2对蠕虫和曼氏血吸虫卵的反应不发展与IRF-4缺陷型DC（IRF-4f/f CD 11 c-cre）的小鼠。常规DC，特别是来自肠的表达CD 11b的DC的连续转移足以引发S。曼氏特异性Th 2应答。令人惊讶的是，转移的IRF-4缺陷型DC也有效地引发S。曼氏特异性Th 2应答。卵抗原不诱导IRF-4相关基因的表达。相反，IRF-4f/f CD 11 c-cre小鼠具有较少的CD 11b+迁移DC和较少的携带寄生虫抗原至淋巴结的DC。此外，CD 11b + CD 103 + DCs在小肠中诱导Th 2应答，而CD 11b + CD 103 − DCs在结肠中发挥这一作用，揭示了肠道DCs在诱导Th 2应答方面的特异性功能异质性。辅助性T细胞2（Th 2）应答对于对抗寄生虫的免疫是必不可少的，但Th 2应答如何在肠道中调节仍不清楚。在这里，作者表明，通过CD 11b，CD 103和IRF 4可区分的不同树突状细胞亚群在小肠或结肠中起促进Th 2应答的作用。
T-helper 2 (Th2) cell responses defend against parasites. Although dendritic cells (DCs) are vital for the induction of T-cell responses, the DC subpopulations that induce Th2 cells in the intestine are unidentified. Here we show that intestinal Th2 responses against Trichuris muris worms and Schistosoma mansoni eggs do not develop in mice with IRF-4-deficient DCs (IRF-4f/f CD11c-cre). Adoptive transfer of conventional DCs, in particular CD11b-expressing DCs from the intestine, is sufficient to prime S. mansoni-specific Th2 responses. Surprisingly, transferred IRF-4-deficient DCs also effectively prime S. mansoni-specific Th2 responses. Egg antigens do not induce the expression of IRF-4-related genes. Instead, IRF-4f/f CD11c-cre mice have fewer CD11b+ migrating DCs and fewer DCs carrying parasite antigens to the lymph nodes. Furthermore, CD11b+CD103+ DCs induce Th2 responses in the small intestine, whereas CD11b+CD103− DCs perform this role in the colon, revealing a specific functional heterogeneity among intestinal DCs in inducing Th2 responses. T helper 2 (Th2) cell responses are essential for immunity against parasites, but how Th2 response is modulated in the gut is still unclear. Here the authors show that distinct dendritic cell subsets distinguishable by CD11b, CD103 and IRF4 function in the small intestine or colon to promote Th2 responses.