{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:33:57Z","timestamp":1792787637754,"version":"4.5.0"},"reference-count":88,"publisher":"American Society for Clinical Investigation","issue":"7","funder":[{"name":"NIH","award":["R01AI077283"],"award-info":[{"award-number":["R01AI077283"]}]},{"name":"NIH","award":["R01AI077283"],"award-info":[{"award-number":["R01AI077283"]}]},{"name":"NIH","award":["R01CA188419"],"award-info":[{"award-number":["R01CA188419"]}]},{"name":"NIH","award":["TL1TR001451"],"award-info":[{"award-number":["TL1TR001451"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,4,5]]},"abstract":"<jats:p>\n                    GARP, a cell surface docking receptor for binding and activating latent TGF-\u03b2, is highly expressed by platelets and activated Tregs. While GARP is implicated in immune invasion in cancer, the roles of the GARP-TGF-\u03b2 axis in systemic autoimmune diseases are unknown. Although B cells do not express GARP at baseline, we found that the GARP-TGF-\u03b2 complex is induced on activated human and mouse B cells by ligands for multiple TLRs, including TLR4, TLR7, and TLR9. GARP overexpression on B cells inhibited their proliferation, induced IgA class-switching, and dampened T cell\u2013independent antibody production. In contrast, B cell\u2013specific deletion of GARP-encoding gene\n                    <jats:italic>Lrrc32<\/jats:italic>\n                    in mice led to development of systemic autoimmune diseases spontaneously as well as worsening of pristane-induced lupus-like disease. Canonical TGF-\u03b2 signaling more readily upregulates GARP in Peyer patch B cells than in splenic B cells. Furthermore, we demonstrated that B cells are required for the induction of oral tolerance of T cell\u2013dependent antigens via GARP. Our studies reveal for the first time to our knowledge that cell surface GARP-TGF-\u03b2 is an important checkpoint for regulating B cell peripheral tolerance, highlighting a mechanism of autoimmune disease pathogenesis.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.99863","type":"journal-article","created":{"date-parts":[[2018,4,4]],"date-time":"2018-04-04T11:00:55Z","timestamp":1522839655000},"source":"Crossref","is-referenced-by-count":51,"title":["B lymphocytes confer immune tolerance via cell surface GARP-TGF-\u03b2 complex"],"prefix":"10.1172","volume":"3","author":[{"given":"Caroline H.","family":"Wallace","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bill X.","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Microbiology and 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