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Contextual control of skin immunity and inflammation by . | LitMetric

Contextual control of skin immunity and inflammation by .

J Exp Med

Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

Published: March 2018

AI Article Synopsis

  • - Researchers found that specific types of skin bacteria significantly increase both the number and activity of a particular type of immune cell called γδ T cells, and this effect lasts over time and doesn't rely on other microbes.
  • - Normally, the skin microbiota's influence is mild and not inflammatory, but it can trigger inflammation when the host is on a high-fat diet, with this process being linked to a molecule called interleukin (IL)-23.
  • - The study highlights a communication pathway between skin bacteria and the immune system, showing that the effects of these bacteria can vary depending on the host's overall health and diet, particularly highlighting the role of mycolic acid in this interaction.

Article Abstract

How defined microbes influence the skin immune system remains poorly understood. Here we demonstrate that , dominant members of the skin microbiota, promote a dramatic increase in the number and activation of a defined subset of γδ T cells. This effect is long-lasting, occurs independently of other microbes, and is, in part, mediated by interleukin (IL)-23. Under steady-state conditions, the impact of is discrete and noninflammatory. However, when applied to the skin of a host fed a high-fat diet, alone promotes inflammation in an IL-23-dependent manner. Such effect is highly conserved among species of and dependent on the expression of a dominant component of the cell envelope, mycolic acid. Our data uncover a mode of communication between the immune system and a dominant genus of the skin microbiota and reveal that the functional impact of canonical skin microbial determinants is contextually controlled by the inflammatory and metabolic state of the host.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5839758PMC
http://dx.doi.org/10.1084/jem.20171079DOI Listing

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