Hashiguchi Masaaki, Kashiwakura Yuji, Kojima Hidefumi, Kobayashi Ayano, Kanno Yumiko, Kobata Tetsuji
Department of Immunology, Dokkyo Medical University School of Medicine, Mibu, Tochigi 321-0293, Japan.
Department of Immunology, Dokkyo Medical University School of Medicine, Mibu, Tochigi 321-0293, Japan.
Immunol Lett. 2015 May;165(1):1-9. doi: 10.1016/j.imlet.2015.03.002. Epub 2015 Mar 17.
Anatomical containment of commensal bacteria in the intestinal mucosa is promoted by innate lymphoid cells (ILCs). However, the mechanism by which ILCs regulate bacterial localization to specific regions remains unknown. Here we show that Peyer's patch (PP) ILCs robustly produce IL-22 and IFN-γ in the absence of exogenous stimuli. Antibiotic treatment of mice decreased both IL-22+ and IFN-γ+ cells in PPs. Blockade of both IL-2 and IL-23 signaling in vitro lowered IL-22 and IFN-γ production. PP ILCs induced mRNA expression of the antibacterial proteins RegIIIβ and RegIIIγ in intestinal epithelial cells. Furthermore, in vivo depletion of ILCs rather than T cells altered bacterial composition and allowed bacterial proliferation in PPs. Collectively, our results show that ILCs regulate the expansion of commensal bacteria in PPs.
固有淋巴细胞（ILC）促进共生细菌在肠道黏膜中的解剖学定位。然而，ILC调节细菌定位于特定区域的机制仍不清楚。在此我们表明，派尔集合淋巴结（PP）中的ILC在无外源性刺激的情况下能大量产生白细胞介素-22（IL-22）和干扰素-γ（IFN-γ）。用抗生素处理小鼠会减少PP中IL-22⁺和IFN-γ⁺细胞的数量。体外阻断IL-2和IL-23信号会降低IL-22和IFN-γ的产生。PP中的ILC诱导肠道上皮细胞中抗菌蛋白RegIIIβ和RegIIIγ的mRNA表达。此外，体内清除ILC而非T细胞会改变细菌组成，并使PP中的细菌增殖。总体而言，我们的结果表明ILC调节PP中共生细菌的扩增。
