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肠道树突状细胞呈递分段丝状菌抗原可驱动黏膜 Th17 细胞分化。

Segmented filamentous bacteria antigens presented by intestinal dendritic cells drive mucosal Th17 cell differentiation.

机构信息

Department of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA.

Center for Biotechnology and Genomic Medicine, Georgia Regents University, Augusta, GA 30912, USA.

出版信息

Immunity. 2014 Apr 17;40(4):594-607. doi: 10.1016/j.immuni.2014.03.005. Epub 2014 Mar 27.

DOI:10.1016/j.immuni.2014.03.005
PMID:24684957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4084624/
Abstract

How commensal microbiota contributes to immune cell homeostasis at barrier surfaces is poorly understood. Lamina propria (LP) T helper 17 (Th17) cells participate in mucosal protection and are induced by commensal segmented filamentous bacteria (SFB). Here we show that MHCII-dependent antigen presentation of SFB antigens by intestinal dendritic cells (DCs) is crucial for Th17 cell induction. Expression of MHCII on CD11c(+) cells was necessary and sufficient for SFB-induced Th17 cell differentiation. Most SFB-induced Th17 cells recognized SFB in an MHCII-dependent manner. SFB primed and induced Th17 cells locally in the LP and Th17 cell induction occurred normally in mice lacking secondary lymphoid organs. The importance of other innate cells was unveiled by the finding that MHCII deficiency in group 3 innate lymphoid cells (ILCs) resulted in an increase in SFB-independent Th17 cell differentiation. Our results outline the complex role of DCs and ILCs in the regulation of intestinal Th17 cell homeostasis.

摘要

共生微生物菌群如何有助于屏障表面免疫细胞的体内平衡尚不清楚。固有层（LP）辅助性 T 细胞 17（Th17）细胞参与黏膜保护，并由共生的分段丝状细菌（SFB）诱导。在这里，我们表明，肠道树突状细胞（DC）对 SFB 抗原的 MHCII 依赖性抗原呈递对于 Th17 细胞的诱导至关重要。CD11c(+)细胞上 MHCII 的表达对于 SFB 诱导的 Th17 细胞分化是必需和充分的。大多数 SFB 诱导的 Th17 细胞以 MHCII 依赖性方式识别 SFB。SFB 在 LP 中诱导和诱导局部 Th17 细胞，而在缺乏次级淋巴器官的小鼠中，Th17 细胞的诱导正常发生。发现 3 组先天淋巴细胞（ILC）中 MHCII 缺陷导致 SFB 非依赖性 Th17 细胞分化增加，揭示了其他先天细胞的重要性。我们的研究结果概述了 DC 和 ILC 在调节肠道 Th17 细胞体内平衡中的复杂作用。

相似文献

[1]
Segmented filamentous bacteria antigens presented by intestinal dendritic cells drive mucosal Th17 cell differentiation.

Immunity. 2014-3-27

[2]
Microbial learning lessons: SFB educate the immune system.

Immunity. 2014-4-17

[3]
Specific microbiota-induced intestinal Th17 differentiation requires MHC class II but not GALT and mesenteric lymph nodes.

J Immunol. 2014-6-4

[4]
Focused specificity of intestinal TH17 cells towards commensal bacterial antigens.

Nature. 2014-4-13

[5]
Segmented filamentous bacterium uses secondary and tertiary lymphoid tissues to induce gut IgA and specific T helper 17 cell responses.

Immunity. 2014-4-17

[6]
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Nature. 2013-5-22

[7]
Group 3 innate lymphoid cells inhibit T-cell-mediated intestinal inflammation through aryl hydrocarbon receptor signaling and regulation of microflora.

Immunity. 2013-8-15

[8]
Intestinal Monocyte-Derived Macrophages Control Commensal-Specific Th17 Responses.

Cell Rep. 2015-8-25

[9]
Redundant cytokine requirement for intestinal microbiota-induced Th17 cell differentiation in draining lymph nodes.

Cell Rep. 2021-8-24

[10]
Constitutive induction of intestinal Tc17 cells in the absence of hematopoietic cell-specific MHC class II expression.

Eur J Immunol. 2013-8-25

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本文引用的文献

[1]
Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation.

Nature. 2013-11-13

[2]
Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells.

Nature. 2013-11-13

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Group 3 innate lymphoid cells inhibit T-cell-mediated intestinal inflammation through aryl hydrocarbon receptor signaling and regulation of microflora.

Immunity. 2013-8-15

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Treg induction by a rationally selected mixture of Clostridia strains from the human microbiota.

Nature. 2013-7-10

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Science. 2013-7-4

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Innate lymphoid cells regulate CD4+ T-cell responses to intestinal commensal bacteria.

Nature. 2013-5-22

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Immunol Cell Biol. 2013-2-12

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Curr Opin Immunol. 2012-5-19

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