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However, whether Treg cells hamper pain at steady state and by which mechanism is still unclear. From a meta-analysis of the transcriptomes of murine Treg and conventional T cells (Tconv), we observe that the proenkephalin gene (\n                    <jats:italic>Penk<\/jats:italic>\n                    ), encoding the precursor of analgesic opioid peptides, ranks among the top 25 genes most enriched in Treg cells. We then present various evidence suggesting that\n                    <jats:italic>Penk<\/jats:italic>\n                    is regulated in part by members of the Tumor Necrosis Factor Receptor (TNFR) family and the transcription factor Basic leucine zipper transcription faatf-like (BATF). Using mice in which the promoter activity of\n                    <jats:italic>Penk<\/jats:italic>\n                    can be tracked with a fluorescent reporter, we also show that\n                    <jats:italic>Penk<\/jats:italic>\n                    expression is mostly detected in Treg and activated Tconv in non-inflammatory conditions in the colon and skin. Functionally, Treg cells proficient or deficient for\n                    <jats:italic>Penk<\/jats:italic>\n                    suppress equally well the proliferation of effector T cells in vitro and autoimmune colitis in vivo. In contrast, inducible ablation of\n                    <jats:italic>Penk<\/jats:italic>\n                    in Treg leads to heat hyperalgesia in both male and female mice. Overall, our results indicate that Treg might play a key role at modulating basal somatic sensitivity in mice through the production of analgesic opioid peptides.\n                  <\/jats:p>","DOI":"10.7554\/elife.91359","type":"journal-article","created":{"date-parts":[[2024,2,1]],"date-time":"2024-02-01T08:25:05Z","timestamp":1706775905000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.91359","source":"Crossref","is-referenced-by-count":7,"title":["Enkephalin-mediated modulation of basal somatic sensitivity by regulatory T cells in mice"],"prefix":"10.7554","volume":"13","author":[{"given":"Nicolas","family":"Aubert","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02en5vm52","id-type":"ROR","asserted-by":"publisher"}],"name":"Centre d\u2019Immunologie et des Maladies Infectieuses (CIMI-PARIS), INSERM, CNRS, Sorbonne Universit\u00e9","place":["Paris, 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