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幽门螺杆菌感染的巨噬细胞诱导 Th17 细胞分化。

Helicobacter pylori-infected macrophages induce Th17 cell differentiation.

机构信息

Department of Clinical Microbiology and Immunology, College of Medical Laboratory Science, Third Military Medical University, Chongqing 400038, PR China.

出版信息

Immunobiology. 2011 Jan-Feb;216(1-2):200-7. doi: 10.1016/j.imbio.2010.05.005. Epub 2010 May 19.

DOI:10.1016/j.imbio.2010.05.005
PMID:21112468
Abstract

Th17 cells represent a novel subset of CD4(+) T cells, which is associated with chronic inflammation. The present study evaluated Th17 cell responses to Helicobacter pylori infection in mouse model and CD4(+) T cell differentiation in response to H. pylori-infected macrophages. Th17 cells were observed in the H. pylori-infected gastric tissue. Co-culture of CD4(+) T cells with H. pylori-infected macrophages elevated IL-17 and IFN-γ secretion, up-regulated retinoid-related orphan receptor gamma t (RORγt) and T box expressed in T cells (T-bet) expression and increased the numbers of Th17 and Th1 cells. The expression of CD40, CD80, and CD86 and the secretion of IL-6, TGF-β1, IL-23, and CCL20 were significantly increased in H. pylori-stimulated macrophages. NF-κB pathway participated in the production of IL-6, IL-23, and CCL20 from macrophages in response to H. pylori, and inhibition of NF-κB pathway of macrophages resulted in less Th17 cell differentiation. Taken together, these results suggest that H. pylori induces Th17 cell differentiation via infected macrophages.

摘要

Th17 细胞代表一种新型的 CD4+T 细胞亚群,与慢性炎症有关。本研究评估了 Th17 细胞对幽门螺杆菌感染的反应在小鼠模型中以及 CD4+T 细胞对幽门螺杆菌感染的巨噬细胞的分化反应。在幽门螺杆菌感染的胃组织中观察到 Th17 细胞。将 CD4+T 细胞与幽门螺杆菌感染的巨噬细胞共培养可增加 IL-17 和 IFN-γ 的分泌,上调维甲酸相关孤儿受体γ t(RORγt)和 T 细胞中表达的 T 框(T-bet)表达,并增加 Th17 和 Th1 细胞的数量。幽门螺杆菌刺激的巨噬细胞中 CD40、CD80 和 CD86 的表达以及 IL-6、TGF-β1、IL-23 和 CCL20 的分泌显著增加。NF-κB 通路参与了巨噬细胞对幽门螺杆菌的反应中 IL-6、IL-23 和 CCL20 的产生,而巨噬细胞 NF-κB 通路的抑制导致 Th17 细胞分化减少。总之,这些结果表明,幽门螺杆菌通过感染的巨噬细胞诱导 Th17 细胞分化。

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