Infectious colitis is one of the most common health issues worldwide. Microfold (M) cells actively transport luminal antigens to gut-associated lymphoid tissue to induce IgA responses; however, it remains unknown whether M cells contribute to the induction of cellular immune responses. Here we report that M cell-dependent antigen transport plays a critical role in the induction of Th1, Th17, and Th22 responses against gut commensals in the steady state. The establishment of commensal-specific cellular immunity was a prerequisite for preventing bacterial dissemination during enteropathogenic Citrobacter rodentium infection. Therefore, M cell-null mice developed severe colitis with increased bacterial dissemination. This abnormality was associated with mucosal barrier dysfunction. These observations suggest that antigen transport by M cells may help maintain gut immune homeostasis by eliciting antigen-specific cellular immune responses.

中文翻译：

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Microfold 细胞依赖性抗原转运通过诱导抗原特异性细胞免疫来减轻感染性结肠炎。

传染性结肠炎是全球最常见的健康问题之一。Microfold (M) 细胞主动将管腔抗原转运至肠道相关淋巴组织以诱导 IgA 反应；然而，M 细胞是否有助于诱导细胞免疫反应仍然未知。在这里，我们报告 M 细胞依赖性抗原转运在稳定状态下诱导针对肠道共生体的 Th1、Th17 和 Th22 反应中起着关键作用。共生特异性细胞免疫的建立是防止肠道致病性柠檬酸杆菌感染期间细菌传播的先决条件。因此，M 细胞缺失小鼠患上了严重的结肠炎，细菌传播增加。这种异常与粘膜屏障功能障碍有关。