AI Article Synopsis
- The immune system is always prepared to recognize and respond to the microbiota, which includes a preexisting pool of T cells specific to these microorganisms, even before any inflammatory trigger occurs.
- In a study using a psoriasis model, exposure to certain commensal skin fungi was found to worsen tissue inflammation due to pre-formed T cell responses.
- The increased inflammation linked to fungal exposure involves specific immune mechanisms (Th17 responses and neutrophil traps) and shares similarities with the gene expression patterns seen in human psoriasis-affected skin.
Article 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7368261 | PMC |
| http://dx.doi.org/10.1073/pnas.2003022117 | DOI Listing |
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