Under steady-state conditions, the immune system is poised to sense and respond to the microbiota. As such, immunity to the microbiota, including T cell responses, is expected to precede any inflammatory trigger. How this pool of preformed microbiota-specific T cells contributes to tissue pathologies remains unclear. Here, using an experimental model of psoriasis, we show that recall responses to commensal skin fungi can significantly aggravate tissue inflammation. Enhanced pathology caused by fungi preexposure depends on Th17 responses and neutrophil extracellular traps and recapitulates features of the transcriptional landscape of human lesional psoriatic skin. Together, our results propose that recall responses directed to skin fungi can directly promote skin inflammation and that exploration of tissue inflammation should be assessed in the context of recall responses to the microbiota.

在稳态条件下，免疫系统可以感知并响应微生物群。这样，预期对微生物群的免疫，包括T细胞应答，将在任何炎症触发之前发生。目前尚不清楚这种预先形成的微生物群特异性T细胞池如何导致组织病理学改变。在这里，我们使用银屑病的实验模型，表明对共生皮肤真菌的召回反应会显着加重组织炎症。由真菌预暴露引起的病理增强取决于Th17反应和嗜中性粒细胞胞外陷阱，并概括了人类皮损皮损的转录特征。一起，