{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T10:17:46Z","timestamp":1788171466756,"version":"build-2803163510"},"reference-count":72,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T00:00:00Z","timestamp":1788134400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01EY034111"],"award-info":[{"award-number":["R01EY034111"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Chronic non-infectious uveitis (NIU) is a vision-threatening inflammatory disease in which relapses often occur despite corticosteroids, conventional immunosuppression, and biologic therapy. A growing body of experimental and human evidence indicates that disease persistence is not explained solely by transient effector inflammation. Instead, autoreactive memory CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells can survive after the initiating trigger and retain retinal antigen responsiveness, sustaining persistent inflammation and reinitiating acute flares and exacerbations. In experimental chronic autoimmune uveitis, a specific subset of CD44\n                    <jats:sup>hi<\/jats:sup>\n                    IL-7R\n                    <jats:sup>+<\/jats:sup>\n                    IL-15R\n                    <jats:sup>+<\/jats:sup>\n                    memory CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells is maintained in the retina and peripheral secondary lymphoid organs (SLO), while additional autoreactive memory cells can persist in bone marrow niches through signal transducer and activator of transcription 3 (STAT3)-dependent mechanisms. Human studies further show expansion of memory and T helper 17 (Th17)-associated CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell populations in NIU; however, the dominant immune cell subsets, clonotypes, and cytokine programs vary among heterogeneous clinical entities of NIU. This review summarizes how memory CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells are generated, maintained, and linked to ocular tissue injury, with emphasis on their effector functions, IL-7 and IL-15-dependent survival signaling, STAT3-linked persistence, trafficking, and failed control by ocular immune regulation. We further discuss memory-directed therapeutic concepts grouped as disruption of survival\/signaling, restraint of trafficking, and immune tolerization or restoration of ocular immune privilege. We propose the hypothesis that, in NIU subsets demonstrably sustained by pathogenic memory CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells, durable remission may require elimination, restraint, or reprogramming of this reservoir rather than suppression of downstream cytokines alone.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1916577","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T09:49:57Z","timestamp":1788169797000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Memory CD4+ T cells in chronic uveitis: pathogenicity, mechanisms, and therapeutic implications"],"prefix":"10.3389","volume":"17","author":[{"given":"Maryam","family":"Shayan","sequence":"first","affiliation":[{"name":"Department of Ophthalmology, Schepens Eye Research Institute of Massachusetts Eye and Ear, Harvard Medical School","place":["Boston, MA, United 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