| Literature DB >> 32601220 |
Charlotte Hurabielle1,2,3, Verena M Link1, Nicolas Bouladoux1,4, Seong-Ji Han1, Eric Dean Merrill1,5, Yaima L Lightfoot6,7, Nickie Seto6, Christopher K E Bleck8, Margery Smelkinson9, Oliver J Harrison1,10, Jonathan L Linehan1,11, Samira Tamoutounour1, Michail S Lionakis12, Mariana J Kaplan6, Saeko Nakajima13,14, Yasmine Belkaid13,4.
Abstract
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.Entities:
Keywords: Th17; fungi; microbiota; psoriasis; skin
Mesh：
Year: 2020 PMID： 32601220 PMCID： PMC7368261 DOI： 10.1073/pnas.2003022117
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205