{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T00:14:27Z","timestamp":1790727267234,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2025,7,19]],"date-time":"2025-07-19T00:00:00Z","timestamp":1752883200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis & Rheumatology"],"published-print":{"date-parts":[[2025,11]]},"abstract":"\n Objective<\/jats:title>\n Autoimmunity occurs due to the tactics between pathogenic and regulatory factors in systemic organs. Although interorgan communication has been demonstrated in various diseases, the effects of the crosstalk between the immune system and other organs on autoimmune disease is unknown.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n We analyzed the influence of interorgan communication on the cellular or molecular mechanism of autoimmunity using a mouse model of primary Sj\u00f6gren disease (pSjD) and patients with pSjD by integrative genomic, bioinformatic, pathologic, and immunologic analyses.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Fibrinogen\u2010like protein\u20101 (FGL\u20101) was identified as a potent factor for interorgan communication between the liver and immune system in pSjD model mice. The production of FGL\u20101 of the liver is induced by interleukin\u20106 (IL\u20106) from CD4\n +<\/jats:sup>\n T cells in these mice. The onset of autoimmune lesions in an\n Fgl1<\/jats:italic>\n \u2010deficient pSjD model mice was earlier than that in the wild type pSjD model mice. FGL\u20101 produced in the liver regulates na\u00efve and memory T cell homeostasis. Further, FGL\u20101 was significantly up\u2010regulated in patients with pSjD compared to the controls. Moreover, its concentration was closely related to the serum IL\u20106 levels in patients with pSjD.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n FGL\u20101 plays a key role in the onset of autoimmunity by suppressing T cell activation in pSjD. Our results will facilitate the development of novel diagnostic or therapeutic strategies targeting the interorgan communication for autoimmune diseases.<\/jats:p>\n \n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/art.43236","type":"journal-article","created":{"date-parts":[[2025,5,21]],"date-time":"2025-05-21T04:19:28Z","timestamp":1747801168000},"page":"1573-1584","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Regulatory Role of FGL<\/scp>\n \u20101 in Interorgan Communication by Controlling T Cell Homeostasis During the Onset of Sj\u00f6gren Disease"],"prefix":"10.1002","volume":"77","author":[{"given":"Kunihiro","family":"Otsuka","sequence":"first","affiliation":[{"name":"Department of Oral Pathology Tokushima University Graduate School of Biomedical Sciences and Department of Interdisciplinary Researches for Medicine and Photonics, 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