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Linehan, J. L., Harrison, O. J., & Han, S.-J. (2018). Non-classical immunity controls microbiota impact on skin immunity and tissue repair. Cell, 172(4), 784–796.e18. Added by: Dr. Enrique Feoli (05/11/2023, 20:36) Last edited by: Dr. Enrique Feoli (06/11/2023, 18:47) |
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| Resource type: Journal Article DOI: https://doi.org/10.1016/j.cell.2017.12.033 ID no. (ISBN etc.): 0092-8674 BibTeX citation key: Linehan2018 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Wound Healing Creators: Han, Harrison, Linehan Collection: Cell |
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Conclusiones
Notably, CD8+ T cells induced by S. epidermidis express high levels of amphiregulin, a molecule described for its mitogenic role on keratinocytes through binding the epidermal growth factor receptor (EGFR) (Werner and Grose, 2003). Additionally, these cells expressed fibroblast growth factor (FGF) family members with previously identified roles as keratinocyte mitogens (Kawano et al., 2005, Werner and Grose, 2003). This production of an EGFR ligand and FGFs by commensal-specific CD8+ T cells supports the idea that these cells may utilize redundant mechanisms to promote tissue repair. We also found that CD8+ T cells induced by S. epidermidis localized to the edge of the wound post-injury, a tropism that may serve the dual purpose of enhancing keratinocyte proliferation while at the same time promoting antimicrobial defense at a site of high vulnerability.
Added by: Dr. Enrique Feoli |
| Abstract |
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Summary Mammalian barrier surfaces are constitutively colonized by numerous microorganisms. We explored how the microbiota was sensed by the immune system and the defining properties of such responses. Here, we show that a skin commensal can induce T cell responses in a manner that is restricted to non-classical MHC class I molecules. These responses are uncoupled from inflammation and highly distinct from pathogen-induced cells. Commensal-specific T cells express a defined gene signature that is characterized by expression of effector genes together with immunoregulatory and tissue-repair signatures. As such, non-classical MHCI-restricted commensal-specific immune responses not only promoted protection to pathogens, but also accelerated skin wound closure. Thus, the microbiota can induce a highly physiological and pleiotropic form of adaptive immunity that couples antimicrobial function with tissue repair. Our work also reveals that non-classical MHC class I molecules, an evolutionarily ancient arm of the immune system, can promote homeostatic immunity to the microbiota.
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