The microbiota colonizes each barrier site and broadly controls host physiology¹. However, when uncontrolled, microbial colonists can also promote inflammation and induce systemic infection². The unique strategies employed at each barrier tissue to control the coexistence of the host with its microbiota remain largely elusive. Here we uncover that, within the skin, host-microbiota symbiosis depends on the remarkable ability of the skin to act as an autonomous lymphoid organ. Notably, an encounter with a new skin commensal promotes two parallel responses, both under the control of Langerhans cells. On one hand, skin commensals induce the formation of classical germinal centers within the lymph node associated with IgG1 and IgG3 antibody responses. On the other hand, microbial colonization also leads to the development of tertiary lymphoid organs within the skin that can locally sustain IgG2b and IgG2c responses. These phenomena are supported by the ability of regulatory T cells to convert into T follicular helper cells. Skin autonomous production of antibodies is sufficient to control local microbial biomass, as well as subsequent systemic infection with the same microbe. Collectively, these results reveal a striking compartmentalization of humoral responses to the microbiota allowing for control of both microbial symbiosis and potential pathogenesis.

微生物群定植于每个屏障位点并广泛控制宿主生理学¹。然而，如果不加以控制，微生物定植剂也会促进炎症并诱导全身感染²。每个屏障组织为控制宿主与其微生物群共存而采用的独特策略在很大程度上仍然难以捉摸。在这里，我们发现，在皮肤内，宿主-微生物群共生取决于皮肤作为自主淋巴器官的非凡能力。值得注意的是，与新的皮肤共生体相遇会促进两种平行反应，两者都在朗格汉斯细胞的控制下。一方面，皮肤共生器官诱导淋巴结内与 IgG1 和 IgG3 抗体反应相关的经典生发中心的形成。另一方面，微生物定植也导致皮肤内三级淋巴器官的发育，这些器官可以在局部维持 IgG2b 和 IgG2c 反应。这些现象得到了调节性 T 细胞转化为滤泡 T 滤泡辅助细胞的能力的支持。皮肤自主产生抗体足以控制局部微生物生物量，以及随后的相同微生物的全身感染。总的来说，这些结果揭示了对微生物群的体液反应的显着划分，从而可以控制微生物共生和潜在的发病机制。