{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T17:04:49Z","timestamp":1786122289417,"version":"build-2736575974"},"reference-count":44,"publisher":"Wiley","issue":"44","license":[{"start":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T00:00:00Z","timestamp":1778544000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T00:00:00Z","timestamp":1778544000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82273159"],"award-info":[{"award-number":["82273159"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82171838"],"award-info":[{"award-number":["82171838"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Ocular adnexal mucosa\u2010associated lymphoid tissue lymphoma (OAML) is driven by both genetic and immune microenvironmental factors, yet its pathogenic mechanisms remain incompletely understood. We previously identified\n                    <jats:italic>IGLL5<\/jats:italic>\n                    as a recurrently mutated gene associated with poor prognosis in OAML. Functional and mechanistic analyses focusing on the S47G and A54G mutants show that these variants enhance association with the CD79A\/CD79B complex, leading to persistent B\u2010cell receptor (BCR) signaling. This signaling is accompanied by upregulation of CXCL10 and CXCL11, increased CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell recruitment, and an exhaustion\u2010associated dysfunctional phenotype that may contribute to an immune\u2010tolerant microenvironment. Pharmacologic inhibition further shows that combined BTK inhibitor and rituximab treatment suppresses IGLL5\u2010associated BCR activation. Together, these findings support a mutation\u2010associated mechanism in a subset of OAML and nominate IGLL5\u2010related signaling as a potential therapeutic vulnerability.\n                  <\/jats:p>","DOI":"10.1002\/advs.202518780","type":"journal-article","created":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T14:45:27Z","timestamp":1778597127000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Decoding IGLL5 Mutation\u2010Mediated BCR Signaling: A Novel Mechanism of CD8\n                    <sup>+<\/sup>\n                    T Cell Exhaustion and Ocular MALT Lymphoma Progression"],"prefix":"10.1002","volume":"13","author":[{"given":"Andi","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Ophthalmology The First Affiliated Hospital with Nanjing Medical University  Nanjing China"},{"name":"Nanjing Medical University  Nanjing 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