{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T18:20:28Z","timestamp":1790965228562,"version":"4.1.0"},"reference-count":90,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,5,3]],"date-time":"2024-05-03T00:00:00Z","timestamp":1714694400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Individuals with Kabuki syndrome present with immunodeficiency; however, how pathogenic variants in the gene encoding the histone-modifying enzyme lysine methyltransferase 2D (KMT2D) lead to immune alterations remain poorly understood. Following up on our prior report of KMT2D-altered integrin expression in B-cells, we performed targeted analyses of KMT2D\u2019s influence on integrin expression in T-cells throughout development (thymocytes through peripheral T-cells) in murine cells with constitutive- and conditional-targeted\n                    <jats:italic>Kmt2d<\/jats:italic>\n                    deletion. Using high-throughput RNA-sequencing and flow cytometry, we reveal decreased expression (both at the transcriptional and translational levels) of a cluster of leukocyte-specific integrins, which perturb aspects of T-cell activation, maturation, adhesion\/localization, and effector function. H3K4me3 ChIP-PCR suggests that these evolutionary similar integrins are under direct control of KMT2D. KMT2D loss also alters multiple downstream programming\/signaling pathways, including integrin-based localization, which can influence T-cell populations. We further demonstrated that KMT2D deficiency is associated with the accumulation of murine CD8\n                    <jats:sup>+<\/jats:sup>\n                    single-positive (SP) thymocytes and shifts in both human and murine peripheral T-cell populations, including the reduction of the CD4\n                    <jats:sup>+<\/jats:sup>\n                    recent thymic emigrant (RTE) population. Together, these data show that the targeted loss of\n                    <jats:italic>Kmt2d<\/jats:italic>\n                    in the T-cell lineage recapitulates several distinct features of Kabuki syndrome-associated immune deficiency and implicates epigenetic mechanisms in the regulation of integrin signaling.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2024.1341745","type":"journal-article","created":{"date-parts":[[2024,5,3]],"date-time":"2024-05-03T00:39:04Z","timestamp":1714696744000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":15,"title":["KMT2D regulates activation, localization, and integrin expression by T-cells"],"prefix":"10.3389","volume":"15","author":[{"given":"Sarah 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