{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T14:18:33Z","timestamp":1773929913885,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2020,7,29]],"date-time":"2020-07-29T00:00:00Z","timestamp":1595980800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Bcl\u20103 is an atypical member of the I\u03baB family that modulates NF\u2010\u03baB activity in nuclei.\n                    <jats:italic>lpr<\/jats:italic>\n                    mice carry the\n                    <jats:italic>lpr<\/jats:italic>\n                    mutation in Fas, resulting in functional loss of this death receptor; they serve as models for lupus erythematosus and autoimmune lymphoproliferation syndrome (ALPS). To explore the biologic roles of Bcl\u20103 in this disease model, we generated BL6\/lpr mice lacking Bcl\u20103. Unlike\n                    <jats:italic>lpr<\/jats:italic>\n                    mice on an MRL background, BL6\/\n                    <jats:italic>lpr<\/jats:italic>\n                    mice present with very mild lupus\u2010 or ALPS\u2010like phenotypes. Bcl\u20103 KO BL6\/\n                    <jats:italic>lpr<\/jats:italic>\n                    mice, however, developed severe splenomegaly, dramatically increased numbers of double negative T cells\u00a0\u2014\u00a0a hallmark of human lupus, ALPS, and MRL\/\n                    <jats:italic>lpr<\/jats:italic>\n                    mice\u00a0\u2014\u00a0and exhibited inflammation in multiple organs, despite low levels of autoantibodies, similar to those in BL6\/\n                    <jats:italic>lpr<\/jats:italic>\n                    mice. Loss of Bcl\u20103 specifically in T cells exacerbated select lupus\u2010like phenotypes, specifically organ infiltration. Mechanistically, elevated levels of Tnf\u03b1 in Bcl\u20103 KO BL6\/\n                    <jats:italic>lpr<\/jats:italic>\n                    mice may promote lupus\u2010like phenotypes, since loss of Tnf\u03b1 in these mice reversed the pathology due to loss of Bcl\u20103. Contrary to the inhibitory functions of Bcl\u20103 revealed here, this regulator has also been shown to promote inflammation in different settings. Our findings highlight the profound, yet highly context\u2010dependent roles of Bcl\u20103 in the development of inflammation\u2010associated pathology.\n                  <\/jats:p>","DOI":"10.1002\/eji.202048584","type":"journal-article","created":{"date-parts":[[2020,7,11]],"date-time":"2020-07-11T17:41:54Z","timestamp":1594489314000},"page":"197-205","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Bcl\u20103 inhibits lupus\u2010like phenotypes in BL6\/\n                    <i>lpr<\/i>\n                    mice"],"prefix":"10.1002","volume":"51","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9887-6905","authenticated-orcid":false,"given":"Wanhu","family":"Tang","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases National Institutes of Health  Bethesda MD 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