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Resolution of chemotherapy-induced peripheral neuropathy (CIPN) after treatment completion depends on CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells and on IL-10 produced by other cells. Using\n                    <jats:italic>Rag2<\/jats:italic>\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice lacking T and B cells and adoptive transfer of\n                    <jats:italic>Il13<\/jats:italic>\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells, we showed that CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells producing IL-13 were required for resolution of CIPN. Intrathecal administration of anti\u2013IL-13 delayed resolution of CIPN and reduced IL-10 production by dorsal root ganglion macrophages. Depleting local CD206\n                    <jats:sup>+<\/jats:sup>\n                    macrophages also delayed resolution of CIPN. In vitro, TIM3\n                    <jats:sup>+<\/jats:sup>\n                    CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells cultured with cisplatin, apoptotic cells, or phosphatidylserine liposomes produced IL-13, which induced IL-10 in macrophages. In vivo, resolution of CIPN was delayed by intrathecal administration of anti-TIM3. Resolution was also delayed in\n                    <jats:italic>Rag2<\/jats:italic>\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice reconstituted with\n                    <jats:italic>Havcr2<\/jats:italic>\n                    (TIM3)\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells. Our data indicated that cell damage induced by cisplatin activated TIM3 on CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells, leading to increased IL-13 production, which in turn induced macrophage IL-10 production and resolution of CIPN. Development of exogenous activators of the IL-13\/IL-10 pain resolution pathway may provide a way to treat the underlying cause of chronic pain.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.154194","type":"journal-article","created":{"date-parts":[[2022,3,7]],"date-time":"2022-03-07T14:00:56Z","timestamp":1646661656000},"source":"Crossref","is-referenced-by-count":91,"title":["CD8+ T cell\u2013derived IL-13 increases macrophage IL-10 to resolve neuropathic pain"],"prefix":"10.1172","volume":"7","author":[{"given":"Susmita K.","family":"Singh","sequence":"first","affiliation":[{"name":"Laboratories of Neuroimmunology, Department of Symptom Research, the University of Texas MD Anderson Cancer Center, Houston, Texas, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen","family":"Krukowski","sequence":"additional","affiliation":[{"name":"Laboratories of Neuroimmunology, Department of Symptom Research, the University of Texas MD Anderson Cancer Center, 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