SignificanceTissues exposed to the environment are sites of exposure to symbiotic microbes including fungi that are continuously sensed by the immune system. Here, we show that immunity to commensal skin fungi can significantly aggravate tissue inflammation. Enhanced pathology caused by fungi preexposure depends on lymphocytes able to produce the cytokine IL-17 and the formation of extracellular traps by neutrophils. We also found that fungal exposure prior to experimental modeling of psoriasis 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.