{"id":62764,"date":"2026-04-28T01:12:27","date_gmt":"2026-04-27T23:12:27","guid":{"rendered":"https:\/\/inmuno.es\/index.php\/2026\/04\/28\/deficiency-of-microrna-10a-in-cd4-t-cells-protects-against-intestinal-infection-through-mitochondrial-oxidation-il-22-pathway\/"},"modified":"2026-04-28T01:12:27","modified_gmt":"2026-04-27T23:12:27","slug":"deficiency-of-microrna-10a-in-cd4-t-cells-protects-against-intestinal-infection-through-mitochondrial-oxidation-il-22-pathway","status":"publish","type":"post","link":"https:\/\/inmuno.es\/index.php\/2026\/04\/28\/deficiency-of-microrna-10a-in-cd4-t-cells-protects-against-intestinal-infection-through-mitochondrial-oxidation-il-22-pathway\/","title":{"rendered":"Deficiency of microRNA-10a in CD4+ T cells protects against intestinal infection through mitochondrial oxidation-IL-22 pathway"},"content":{"rendered":"<div>\n<p><b>J Immunol<\/b>. 2026 Apr 15;215(4):vkag089. doi: 10.1093\/jimmun\/vkag089.<\/p>\n<p><b>ABSTRACT<\/b><\/p>\n<p>Interleukin 22 (IL-22) produced by CD4+ T cells plays an important role in regulating intestinal immune responses during inflammation and infection, but the mechanisms controlling IL-22 expression in T cells remain incompletely understood. MicroRNA-10a (miR-10a) is known to regulate CD4+ T-cell function, but its role in IL-22 production has not been defined. Here, using mouse CD4+ T cell-specific miR-10a knockout models, we examined how miR-10a regulates IL-22 expression and the underlying metabolic mechanisms. MiR-10a deficiency led to increased IL-22 production in CD4+ T cells both in vitro and in vivo, under steady and inflammatory conditions. CD4+ T cell-specific miR-10a knockout mice were resistant to Citrobacter rodentium infection, and the protection was abolished when blocking the IL-22 pathway in mice. Mechanistically, miR-10a-deficient CD4+ T cells exhibited increased mitochondrial oxidative metabolism and membrane potential. Pharmacologic inhibition of mitochondrial complex III with antimycin A suppressed the enhanced IL-22 production in miR-10a-deficient T cells. We further identified Uqcrq, a subunit of mitochondrial complex III, as a direct target of miR-10a, and loss of Uqcrq suppressed IL-22 production in CD4+ T cells. Together, these findings identify miR-10a as a T cell-intrinsic regulator of mitochondrial oxidative metabolism that constrains IL-22 production in the intestine.<\/p>\n<p>PMID:<a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/42044496\/?utm_source=SimplePie&amp;utm_medium=rss&amp;utm_content=2985117R&amp;ff=20260427191227&amp;v=2.19.0.post6+133c1fe\">42044496<\/a> | DOI:<a href=\"https:\/\/doi.org\/10.1093\/jimmun\/vkag089\">10.1093\/jimmun\/vkag089<\/a><\/p>\n<\/div>","protected":false},"excerpt":{"rendered":"<p>J Immunol. 2026 Apr 15;215(4):vkag089. doi: 10.1093\/jimmun\/vkag089. ABSTRACT Interleukin 22 (IL-22) produced by CD4+ T cells plays an important role in regulating intestinal immune responses during inflammation and infection, but the mechanisms controlling IL-22 expression in T cells remain incompletely understood. MicroRNA-10a (miR-10a) is known to regulate CD4+ T-cell function, but its role in IL-22 &#8230; <a title=\"Deficiency of microRNA-10a in CD4+ T cells protects against intestinal infection through mitochondrial oxidation-IL-22 pathway\" class=\"read-more\" href=\"https:\/\/inmuno.es\/index.php\/2026\/04\/28\/deficiency-of-microrna-10a-in-cd4-t-cells-protects-against-intestinal-infection-through-mitochondrial-oxidation-il-22-pathway\/\" aria-label=\"Read more about Deficiency of microRNA-10a in CD4+ T cells protects against intestinal infection through mitochondrial oxidation-IL-22 pathway\">Read more<\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[42,71],"tags":[],"class_list":["post-62764","post","type-post","status-publish","format-standard","hentry","category-publicaciones","category-the-journal-of-immunology"],"_links":{"self":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts\/62764","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/comments?post=62764"}],"version-history":[{"count":0,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts\/62764\/revisions"}],"wp:attachment":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/media?parent=62764"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/categories?post=62764"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/tags?post=62764"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}