{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T17:25:05Z","timestamp":1787505905844,"version":"build-2736575974"},"reference-count":69,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T00:00:00Z","timestamp":1767830400000},"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. Pharmacol."],"abstract":"<jats:p>\n                    Integrins are pivotal adhesion receptors that mediate dynamic communication between cells and their surrounding environment. Through bidirectional signaling, they regulate key physiological processes such as cell migration, inflammation, and tissue organization. Among them, the \u03b14 integrin subunit, encoded by the\n                    <jats:italic>ITGA4<\/jats:italic>\n                    gene, forms \u03b14\u03b21 (VLA-4) and \u03b14\u03b27 heterodimers, both essential for leukocyte adhesion and migration across inflamed tissues and blood\u2013brain barrier. Variability in therapeutic response to \u03b14 integrin inhibitors, such natalizumab, highlights the need to clarify the genetic and molecular determinants that regulate\n                    <jats:italic>ITGA4<\/jats:italic>\n                    function. This mini review provides an updated overview of\n                    <jats:italic>ITGA4<\/jats:italic>\n                    from historical, biological, and pharmacogenetic perspectives. We summarize current evidence linking\n                    <jats:italic>ITGA4<\/jats:italic>\n                    genetic variants with disease susceptibility, progression, and therapeutic outcomes in autoimmune and neuroinflammatory disorders. Finally, we discuss existing limitations, population inconsistencies, and emerging strategies integrating multi-omic and\n                    <jats:italic>in silico<\/jats:italic>\n                    analyses to translate\n                    <jats:italic>ITGA4<\/jats:italic>\n                    variants into predictive biomarkers for personalized immunotherapy.\n                  <\/jats:p>","DOI":"10.3389\/fphar.2025.1745315","type":"journal-article","created":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T06:34:06Z","timestamp":1767854046000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["ITGA4 genetic variants as a predictor of therapeutic responsivity to autoimmune diseases"],"prefix":"10.3389","volume":"16","author":[{"given":"Matheus D.","family":"De Matos","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B\u00e1rbara D.","family":"Guimenes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giovanni K.","family":"Pavani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriel Gripp","family":"Fernandes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guilherme C.","family":"Montes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabr\u00edcia L.","family":"Fontes-Dantas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,1,8]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"349","DOI":"10.54029\/2023afn","article-title":"Integrin alpha-4 gene polymorphism in relation to natalizumab response in multiple sclerosis patients","volume":"28","author":"Ahmed","year":"","journal-title":"Neurol. 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