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      An ocular commensal protects against corneal infection by driving an Interleukin 17 response from mucosal γδ T cells

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          Summary

          Mucosal sites such as the intestine, oral cavity, nasopharynx, and vagina all have associated commensal flora. The surface of the eye is also a mucosal site, but proof of a living, resident ocular microbiome remains elusive. Here, we used a mouse model of ocular surface disease to reveal that commensals were present in the ocular mucosa and had functional immunological consequences. We isolated one such candidate commensal, Corynebacterium mastitidis and showed that this organism elicited a commensal-specific interleukin 17 response from γδ T cells in the ocular mucosa that was central to local immunity. The commensal-specfic response drove neutrophil recruitment and the release of antimicrobials into the tears, and protected the eye from pathogenic Candida albicans or Pseudomonas aeruginosa infection. Our findings provide direct evidence that a resident commensal microbiome exists on the ocular surface and identify the cellular mechanisms underlying its effects on ocular immune homeostasis and host defense.

          Graphical abstract

          Although the eye is a mucosal site, there has been a long-standing controversy regarding whether a resident microbiome exists on the ocular surface. St. Leger et al. show that a microorganism that lives on the conjunctiva tunes local mucosal immunity and protects the eye from pathogenic infection.

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          Author and article information

          Journal
          9432918
          8591
          Immunity
          Immunity
          Immunity
          1074-7613
          1097-4180
          1 July 2017
          11 July 2017
          18 July 2017
          18 July 2018
          : 47
          : 1
          : 148-158.e5
          Affiliations
          [1 ]Laboratory of Immunology, National Eye Institute, National Institutes of Health
          [2 ]Fungal Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
          [3 ]Department of Medicine, Division of Infectious Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
          [4 ]Center for Experimental Animal Models, Institute for Medical Sciences, Tokyo University of Science, Tokyo, Japan
          Author notes
          [* ]Correspondence to: Rachel R Caspi ( caspir@ 123456mail.nih.gov ), Laboratory of Immunology, National Eye Institute, National Institutes of Health, 10 Center Drive, 10/10N218, Bethesda, MD 20892-1857, USA, TEL: 1-301-435-4555
          [5]

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          Article
          PMC5553552 PMC5553552 5553552 nihpa887951
          10.1016/j.immuni.2017.06.014
          5553552
          28709803
          b4c7d821-8573-4de0-9261-8269cb12c5a2
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