{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T13:23:50Z","timestamp":1791897830491,"version":"4.3.4"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2025,1,6]],"date-time":"2025-01-06T00:00:00Z","timestamp":1736121600000},"content-version":"vor","delay-in-days":2016,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Ets1 is emerging as a key transcription factor that is required to prevent autoimmunity in mice and humans. Ets1 is expressed in both B and T cells, and mice lacking Ets1 are characterized by excess B and T cell activation, leading to enhanced formation of Ab-secreting cells and high titers of autoantibodies. In humans, genome-wide association studies have detected associations of single nucleotide polymorphisms in the human ETS1 gene with autoimmune diseases, including lupus. An increased fraction of CD4+ T cells from Ets1\u2212\/\u2212 mice have an activated effector-memory phenotype, and there are aberrations in differentiation that contribute to the autoimmune phenotype. In vitro studies of B cells suggest that Ets1 may have B cell\u2013intrinsic effects as well. To confirm B cell\u2013intrinsic roles for Ets1, we crossed CD19-Cre mice to mice with a floxed allele of Ets1. Mice with a B cell\u2013specific deletion of Ets1 show increases in B cell activation, numbers of Ab-secreting cells, and levels of autoantibodies, despite the fact that T cells are normal. However, when compared with conventional Ets1 knockout mice, mice with B cell\u2013specific loss of Ets1 have a significantly milder phenotype. These results demonstrate that Ets1 is required in B cells to prevent autoimmune responses but that loss of Ets1 activity in other cell types is required for maximal autoimmune phenotypes.<\/jats:p>","DOI":"10.4049\/immunohorizons.1900033","type":"journal-article","created":{"date-parts":[[2019,7,17]],"date-time":"2019-07-17T21:55:13Z","timestamp":1563400513000},"page":"331-340","source":"Crossref","is-referenced-by-count":28,"title":["Ets1 Controls the Development of B Cell Autoimmune Responses in a Cell-Intrinsic Manner"],"prefix":"10.1093","volume":"3","author":[{"given":"Alex","family":"Sunshine","sequence":"first","affiliation":[{"name":"Department of Biochemistry, State University of New York at Buffalo , Buffalo, NY 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3271-218X","authenticated-orcid":false,"given":"David","family":"Goich","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, State University of New York at Buffalo , Buffalo, NY 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3559-3654","authenticated-orcid":false,"given":"Alifa","family":"Stith","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, State University of New York at Buffalo , Buffalo, NY 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine","family":"Sortino","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, State University of New York at Buffalo , Buffalo, NY 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin","family":"Dalton","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, State University of New York at Buffalo , Buffalo, NY 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Metcalfe","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, State University of New York at Buffalo , Buffalo, NY 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric C","family":"Svensson","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, University of Chicago , Chicago, IL 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7806-4352","authenticated-orcid":false,"given":"Lee Ann","family":"Garrett-Sinha","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, State University of New York at Buffalo , Buffalo, NY 14203"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,7,18]]},"reference":[{"key":"2025010608414898100_r1","doi-asserted-by":"crossref","first-page":"754","DOI":"10.1016\/j.autrev.2012.02.001","article-title":"Updated assessment of the prevalence, spectrum and case definition of autoimmune disease","volume":"11","author":"Hayter","year":"2012","journal-title":"Autoimmun. 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