{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,10]],"date-time":"2026-11-10T21:02:53Z","timestamp":1794344573366,"version":"4.9.0"},"reference-count":280,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,2]],"date-time":"2026-03-02T00:00:00Z","timestamp":1772409600000},"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. Med."],"abstract":"<jats:p>Uveitis encompasses a heterogeneous group of intraocular inflammatory disorders and remains a leading cause of preventable visual loss. Its immunopathogenesis reflects the interplay between a uniquely regulated ocular environment and triggers that breach or bypass that privilege. Much of our mechanistic understanding derives from animal models, which have helped define key features of ocular immune regulation. Layered mechanisms normally restrain inflammation: physical barriers (blood\u2013aqueous and blood\u2013retina), a locally immunosuppressive milieu, and systemic tolerance circuits such as anterior chamber\u2013associated immune deviation. When these controls fail, disease emerges through a number of broad pathways. In autoimmune uveitis, genetic susceptibility (HLA class I\/II and peptide-trimming enzymes such as ERAP) shapes antigen display and lowers activation thresholds for autoreactive T-cells. Antigen presentation in draining nodes primes Th1\/Th17 responses. Within the eye, effector T-cells are restimulated by resident microglia and recruited macrophages, driving cytokine cascades that disrupt the blood\u2013retina barrier and amplify leukocyte recruitment. B cells may augment tissue injury via antigen presentation, cytokine production, local antibody formation, and, in some entities, ectopic lymphoid structures. These mechanisms are largely defined in experimental autoimmune uveitis and form the basis for extrapolating human pathogenesis. Tissue-resident memory T-cells persist into remission and may influence relapse risk. Autoinflammatory uveitis arises from dysregulated innate pathways independent of antigen specificity. Infectious uveitis reflects direct intraocular infection or reactivation. Post-infectious inflammation may be sustained by antigen persistence or molecular mimicry. Paraneoplastic uveitis (autoimmune retinopathy) arises when anti-tumour immunity cross-reacts with retinal antigens. Therapy should mirror the dominant immunopathology. In infectious uveitis, clinicians first reduce pathogen load with targeted antimicrobials and then add anti-inflammatory therapy under antimicrobial cover; maintenance antivirals curb reactivation when indicated. In autoimmune disease, where Th1\/Th17\u2013macrophage circuits dominate, steroid-sparing treatment targets TNF and IL-6 pathways. In autoinflammatory forms, excess inflammasome\/IL-1 signalling supports IL-1 blockade. Advances in humanised modelling will be key to defining condition-specific mechanisms and supporting the evolution of tailored interventions.<\/jats:p>","DOI":"10.3389\/fmed.2026.1717056","type":"journal-article","created":{"date-parts":[[2026,3,2]],"date-time":"2026-03-02T05:21:19Z","timestamp":1772428879000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":9,"title":["The Immunopathogenesis of uveitis"],"prefix":"10.3389","volume":"13","author":[{"given":"Jimin","family":"Han","sequence":"first","affiliation":[{"name":"Academic Unit of Ophthalmology, Translational Health Sciences","place":["Bristol, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Harper","sequence":"additional","affiliation":[{"name":"Academic Unit of Ophthalmology, Translational Health Sciences","place":["Bristol, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Copland","sequence":"additional","affiliation":[{"name":"Academic Unit of Ophthalmology, Translational Health Sciences","place":["Bristol, United Kingdom"]},{"name":"National Institute of Health Research (NIHR) Moorfields Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology","place":["London, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Panayiotis","family":"Maghsoudlou","sequence":"additional","affiliation":[{"name":"Academic Unit of Ophthalmology, Translational Health Sciences","place":["Bristol, United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,2]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"419","DOI":"10.1001\/jama.2025.4358","article-title":"Uveitis in adults: a review","volume":"334","author":"Maghsoudlou","year":"2025","journal-title":"JAMA"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"2","DOI":"10.1080\/09273948.2016.1196713","article-title":"A focus on the epidemiology of uveitis","volume":"26","author":"Tsirouki","year":"2018","journal-title":"Ocul Immunol Inflamm"},{"key":"ref3","doi-asserted-by":"publisher","first-page":"263","DOI":"10.1076\/ocii.10.4.263.15592","article-title":"Uveitis: a global perspective","volume":"10","author":"Chang","year":"2002","journal-title":"Ocul Immunol Inflamm"},{"key":"ref4","doi-asserted-by":"publisher","first-page":"1930","DOI":"10.1080\/09273948.2023.2282610","article-title":"Uveitis associated with monogenic autoinflammatory syndromes in children","volume":"31","author":"Maghsoudlou","year":"2023","journal-title":"Ocul Immunol Inflamm"},{"key":"ref5","doi-asserted-by":"publisher","first-page":"148","DOI":"10.3389\/fimmu.2012.00148","article-title":"Ocular immune privilege and ocular melanoma: parallel universes or immunological plagiarism?","volume":"3","author":"Niederkorn","year":"2012","journal-title":"Front Immunol"},{"key":"ref6","doi-asserted-by":"crossref","first-page":"385","DOI":"10.1016\/B978-0-12-370454-2.00029-6","article-title":"Chapter twenty-nine - NK cells in the eye","volume-title":"Natural killer cells","author":"Niederkorn","year":"2010"},{"key":"ref7","doi-asserted-by":"publisher","first-page":"680","DOI":"10.1016\/j.survophthal.2016.04.006","article-title":"Autoimmune disease: conceptual history and contributions of ocular immunology","volume":"61","author":"Margo","year":"2016","journal-title":"Surv Ophthalmol"},{"key":"ref8","doi-asserted-by":"publisher","first-page":"50","DOI":"10.1159\/000099253","article-title":"Immune privilege and angiogenic privilege of the cornea","volume":"92","author":"Cursiefen","year":"2007","journal-title":"Chem Immunol Allergy"},{"key":"ref9","doi-asserted-by":"publisher","first-page":"6529","DOI":"10.1167\/iovs.11-7454","article-title":"Combined blockade of VEGFR-3 and VLA-1 markedly promotes high-risk corneal transplant survival","volume":"52","author":"Zhang","year":"2011","journal-title":"Invest Ophthalmol Vis Sci"},{"key":"ref10","doi-asserted-by":"publisher","first-page":"2262","DOI":"10.4049\/jimmunol.157.6.2262","article-title":"Peptide-specific T cell clonal expansion in vivo following immunization in the eye, an immune-privileged site","volume":"157","author":"Egan","year":"1996","journal-title":"J Immunol"},{"key":"ref11","doi-asserted-by":"publisher","first-page":"1885","DOI":"10.1038\/eye.2008.382","article-title":"Ocular immune privilege","volume":"23","author":"Taylor","year":"2009","journal-title":"Eye"},{"key":"ref12","doi-asserted-by":"crossref","first-page":"809","DOI":"10.4049\/jimmunol.118.3.809","article-title":"Immune response to immunization via the anterior chamber of the eye. 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