{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T17:27:55Z","timestamp":1789752475136,"version":"4.0.1"},"reference-count":50,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2021,6,27]],"date-time":"2021-06-27T00:00:00Z","timestamp":1624752000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2021,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Polymorphisms in TACI, a BAFF family cytokine receptor, are linked to diverse human immune disorders including common variable immunodeficiency (CVID) and systemic lupus erythematosus (SLE). Functional studies of individual variants show modest impacts on surface TACI expression and\/or downstream signal transduction, indicating that relatively subtle variation in TACI activity can impact human B\u2010cell biology. However, significant complexity underlies TACI biology, including both positive and negative regulation of physiologic and pathogenic B\u2010cell responses. To model these contradictory events, we compared the functional impact of TACI deletion on separate models of murine SLE driven by T cell\u2010independent and \u2010dependent breaks in B\u2010cell tolerance. First, we studied whether reduced surface TACI expression was sufficient to protect against progressive BAFF\u2010mediated systemic autoimmunity. Strikingly, despite a relatively modest impact on surface TACI levels, TACI haploinsufficiency markedly reduced pathogenic RNA\u2010associated autoantibody titers and conferred long\u2010term protection from BAFF\u2010driven lupus nephritis. In contrast, B cell\u2010intrinsic TACI deletion exerted a limited impact of autoantibody generation in murine lupus characterized by spontaneous germinal center formation and T cell\u2010dependent humoral autoimmunity. Together, these combined data provide new insights into TACI biology and highlight how TACI signals must be tightly regulated during protective and pathogenic B\u2010cell responses.<\/jats:p>","DOI":"10.1002\/eji.202149244","type":"journal-article","created":{"date-parts":[[2021,6,19]],"date-time":"2021-06-19T09:25:45Z","timestamp":1624094745000},"page":"2225-2236","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["TACI haploinsufficiency protects against BAFF\u2010driven humoral autoimmunity in mice"],"prefix":"10.1002","volume":"51","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3250-8258","authenticated-orcid":false,"given":"Holly M.","family":"Jacobs","sequence":"first","affiliation":[{"name":"Seattle Children's Research Institute  Seattle WA 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