Science· 2012Q1
Compartmentalized Control of Skin Immunity by Resident Commensals
- 1,086citations
- Q1SCImago
- 2012year
Short summary
Skin-resident commensal bacteria autonomously control local inflammation and T cell function, establishing distinct immune compartments separate from the gut microbiota.
AI-generated from the title and abstract; the full text is not read.
Key points
- Skin commensals autonomously control local skin inflammation and T cell function.
- Protective immunity to skin pathogens depends on skin microbiota, not gut microbiota.
- Skin commensals tune T cell function via interleukin-1 receptor signaling.
- Tissue-resident commensals create distinct immune compartments.
AI-generated from the title and abstract; the full text is not read.
Abstract
Intestinal commensal bacteria induce protective and regulatory responses that maintain host-microbial mutualism. However, the contribution of tissue-resident commensals to immunity and inflammation at other barrier sites has not been addressed. We found that in mice, the skin microbiota have an autonomous role in controlling the local inflammatory milieu and tuning resident T lymphocyte function. Protective immunity to a cutaneous pathogen was found to be critically dependent on the skin microbiota but not the gut microbiota. Furthermore, skin commensals tuned the function of local T cells in a manner dependent on signaling downstream of the interleukin-1 receptor. These findings underscore the importance of the microbiota as a distinctive feature of tissue compartmentalization, and provide insight into mechanisms of immune system regulation by resident commensal niches in health and disease.
The authors' abstract, as published at the source. Science, 2012 · DOI ↗
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Field: Dermatology
DermatologyMedicine