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The pleiotropic cytokine interleukin-4 (IL-4) has been shown to suppress neuropathic pain in rodent models, but its underlying mechanism remains unclear. Here, we show that intrathecal administration of IL-4 to mice with spinal nerve transection (SpNT) increased the number of CD11c\n                    <jats:sup>+<\/jats:sup>\n                    microglia (a microglia subset important for pain remission) in the spinal dorsal horn (SDH) and that this effect of IL-4 was essential for its ameliorating effect on SpNT-induced pain hypersensitivity. Furthermore, in mice with spared nerve injury (SNI), another model in which pain remission does not occur, the emergence of CD11c\n                    <jats:sup>+<\/jats:sup>\n                    SDH microglia was curtailed, but intrathecal IL-4 increased their emergence and ameliorated pain hypersensitivity in a CD11c\n                    <jats:sup>+<\/jats:sup>\n                    microglia-dependent manner. Our study reveals a mechanism by which intrathecal IL-4 ameliorates pain hypersensitivity after nerve injury and provides evidence that IL-4 increases CD11c\n                    <jats:sup>+<\/jats:sup>\n                    microglia with a function that ameliorates neuropathic pain.\n                  <\/jats:p>","DOI":"10.7554\/elife.105087","type":"journal-article","created":{"date-parts":[[2025,2,7]],"date-time":"2025-02-07T10:25:13Z","timestamp":1738923913000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.105087","source":"Crossref","is-referenced-by-count":2,"title":["Interleukin-4 induces CD11c+ microglia leading to amelioration of neuropathic pain in mice"],"prefix":"10.7554","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5038-5680","authenticated-orcid":true,"given":"Keita","family":"Kohno","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00p4k0j84","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular and System 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