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As epoxy-fatty acids (EpFAs) are degraded by the enzyme soluble epoxide hydrolase (sEH), the inhibition of sEH increases endogenous EpFA levels to promote the resolution of cancer-associated inflammation. Here, we demonstrate that systemic treatment with ICI induces sEH expression in multiple murine cancer models. Dietary omega-3 polyunsaturated fatty acid supplementation and pharmacologic sEH inhibition, both alone and in combination, significantly enhance anti-tumor activity of ICI in these models. Notably, pharmacological abrogation of the sEH pathway alone or in combination with ICI counter-regulates an ICI-induced pro-inflammatory and pro-tumorigenic cytokine storm. Thus, modulating endogenous EpFA levels through dietary supplementation or sEH inhibition may represent a unique strategy to enhance the anti-tumor activity of paradigm cancer therapies.<\/jats:p>","DOI":"10.1073\/pnas.2314085121","type":"journal-article","created":{"date-parts":[[2024,2,8]],"date-time":"2024-02-08T13:40:36Z","timestamp":1707399636000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":30,"title":["Enhancing cancer immunotherapy via inhibition of soluble epoxide hydrolase"],"prefix":"10.1073","volume":"121","author":[{"given":"Abigail G.","family":"Kelly","sequence":"first","affiliation":[{"name":"Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215"},{"name":"Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215"},{"name":"Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, 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