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首页> 外文期刊>Infection and immunity >Helicobacter pylori-Specific CD4+ CD25high Regulatory T Cells Suppress Memory T-Cell Responses to H. pylori in Infected Individuals
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Helicobacter pylori-Specific CD4+ CD25high Regulatory T Cells Suppress Memory T-Cell Responses to H. pylori in Infected Individuals

机译：幽门螺杆菌特异的CD4 + CD25high调节性T细胞抑制感染个体对幽门螺杆菌的记忆T细胞反应

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Helicobacter pylori colonizes the gastric and duodenal mucosa. The infection normally persists for life and causes peptic ulcers and gastric cancer in a subset of infected individuals. We hypothesized that the inability to clear the infection may be a consequence of H. pylori-specific regulatory T cells that actively suppress T-cell responses. Therefore, we characterized the T-cell responses to H. pylori in H. pylori-infected individuals without any subjective symptoms and in uninfected control subjects and investigated the role of regulatory CD4+ CD25high T cells during infection. The stimulation of CD4+ peripheral blood T cells with monocyte-derived dendritic cells pulsed with a membrane preparation of H. pylori resulted in proliferation and gamma interferon production in both infected and uninfected individuals. Sorted memory cells from infected individuals responded less than cells from uninfected subjects, and the unresponsiveness could be abolished by depletion of CD4+ CD25high regulatory T cells or the addition of interleukin 2. Furthermore, CD4+ CD25high T cells suppressed H. pylori-induced responses in cocultures with CD25low/? cells. Tetanus toxoid induced comparable responses in memory cells from infected and uninfected individuals in both the presence and the absence of regulatory T cells, suggesting that the suppression was H. pylori specific. In conclusion, we have shown that H. pylori-infected individuals have impaired memory CD4+ T-cell responses to H. pylori that are linked to the presence of H. pylori-specific regulatory T cells that actively suppress the responses.
机译：幽门螺杆菌 幽门螺旋杆菌定植于胃和十二指肠粘膜。这种感染通常会持续一生，并在一部分感染者中引起消化性溃疡和胃癌。我们假设无法清除感染可能是 H 的结果。幽门螺杆菌特异的调节性T细胞，可主动抑制T细胞反应。因此，我们表征了T细胞对 H 的反应。 H 中的 pylori 。没有任何主观症状且未感染对照受试者的被幽门螺杆菌感染的个体，并研究了感染期间调节性CD4 + CD25 高 T细胞的作用。用 H 膜制剂脉冲单核细胞衍生的树突状细胞刺激CD4 + 外周血T细胞。幽门螺杆菌在受感染和未感染的个体中均导致增殖和γ干扰素产生。来自受感染个体的分类记忆细胞对反应的反应性低于未受感染个体的细胞，并且无反应性可以通过耗尽CD4 + CD25 高调节性T细胞或添加白介素2来消除。此外，CD4 + CD25 高 T细胞抑制了 H 。 CD25 low /？细胞共培养中 pylori 诱导的应答。在存在和不存在调节性T细胞的情况下，破伤风类毒素都能在感染和未感染个体的记忆细胞中诱导相似的反应，表明抑制作用是 H 。 pylori 特定。总之，我们证明了 H 。感染了幽门螺杆菌的个体的记忆CD4 + T细胞对 H 的反应受损。 pylori 与 H 的存在相关。幽门螺杆菌特异的调节性T细胞，可主动抑制反应。

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