{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T00:15:03Z","timestamp":1785888903229,"version":"3.56.0"},"reference-count":50,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,1,8]],"date-time":"2021-01-08T00:00:00Z","timestamp":1610064000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Systemic lupus erythematosus (SLE) is an autoimmune disease that can present with many different permutations of symptom presentation. A large subset of SLE patients have been shown to present with elevated  interferon stimulated gene (ISG) expression, and Type I IFNs (IFN\u03b1\u03b2) have been shown to drive disease in murine models through global IFN\u03b1 Receptor (IFNAR) knockouts. However, the disease contribution of distinct immune cell subsets in response to constitutively increased levels of IFN\u03b1\u03b2 is not fully understood. We utilized a B-cell specific IFNAR knockout (B\u0394IFNAR) on the B6.Nba2 spontaneous-lupus background to determine the contribution of IFN\u03b1\u03b2 stimulated B cells in disease. We found that IFN\u03b1\u03b2 signaling in B cells is driving increased splenomegaly, increased populations of activated B cells, and increased populations of germinal center (GC) B cells, memory B cells, and plasma blasts\/cells, but did not affect the development of glomerulonephritis and immune-complex deposition. IFNAR expression by B cells also drove production of anti-chromatin IgG, and anti-dsDNA and -nRNP IgG and IgG<jats:sub>2C<\/jats:sub> auto-antibody levels, as well as increased <jats:italic>Bcl2<\/jats:italic> expression, affecting GC B cell survival in B6.Nba2 mice.<\/jats:p>","DOI":"10.3389\/fimmu.2020.616064","type":"journal-article","created":{"date-parts":[[2021,1,9]],"date-time":"2021-01-09T13:51:26Z","timestamp":1610200286000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":14,"title":["Partial Protection From Lupus-Like Disease by B-Cell Specific Type I Interferon Receptor Deficiency"],"prefix":"10.3389","volume":"11","author":[{"given":"Emma J.","family":"Keller","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neeva B.","family":"Patel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madeline","family":"Patt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jane K.","family":"Nguyen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Trine N.","family":"J\u00f8rgensen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,1,8]]},"reference":[{"key":"B1","article-title":"How does quality of life of patients with systemic lupus erythematosus compare with that of other common chronic illnesses","volume":"32","author":"Jolly","year":"2005","journal-title":"J\u00a0Rheumatol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1080\/14740338.2019.1685978","article-title":"The safety of belimumab for the treatment of systemic lupus erythematosus","volume":"18","author":"Wise","year":"2019","journal-title":"Expert Opin Drug Saf"},{"key":"B3","doi-asserted-by":"publisher","first-page":"e000280","DOI":"10.1136\/lupus-2018-000280","article-title":"SLE: Reconciling heterogeneity","volume":"6","author":"Lockshin","year":"2019","journal-title":"Lupus Sci Med"},{"key":"B4","doi-asserted-by":"publisher","first-page":"5","DOI":"10.1056\/NEJM197907053010102","article-title":"Immune Interferon in the Circulation of Patients with Autoimmune Disease","volume":"301","author":"Hooks","year":"1979","journal-title":"N Engl J Med"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1191\/096120300674499064","article-title":"Activation of type I interferon system in systemic lupus erythematosus correlates with disease activity but not with antiretroviral antibodies","volume":"9","author":"Bengtsson","year":"2000","journal-title":"Lupus"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2004.033753","article-title":"Type I interferon correlates with serological and clinical manifestations of SLE","volume":"64","author":"Dall\u2019Era","year":"2005","journal-title":"Ann Rheum Dis"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20021553","article-title":"Interferon and granulopoiesis signatures in systemic lupus erythematosus blood","volume":"197","author":"Bennett","year":"2003","journal-title":"J Exp Med"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1186\/ar1015","article-title":"Microarray analysis of gene expression in lupus","volume":"5","author":"Crow","year":"2003","journal-title":"Arthritis Res Ther"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0337679100","article-title":"Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus","volume":"100","author":"Baechler","year":"2003","journal-title":"Proc Natl Acad Sci U S A"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gene.6363966","article-title":"Analysis of gene expression profiles in human systemic lupus erythematosus using oligonucleotide microarray","volume":"4","author":"Han","year":"2003","journal-title":"Genes Immun"},{"key":"B11","article-title":"Risk of autoimmune complications associated with interferon therapy","volume":"8","author":"Silva","year":"2020","journal-title":"Gastroenterol Hepatol (N Y)"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-115-3-178","article-title":"Autoimmunity after alpha-interferon therapy for malignant carcinoid tumors","volume":"115","author":"Ronnblom","year":"1991","journal-title":"Ann Intern Med"},{"key":"B13","article-title":"A monoclonal antibody to recombinant human IFN-alpha receptor inhibits biologic activity of several species of human IFN-alpha, IFN-beta, and IFN-omega. 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