{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T09:52:56Z","timestamp":1790157176924,"version":"4.0.1"},"reference-count":67,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R37AI128901"],"award-info":[{"award-number":["R37AI128901"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Emerging evidence from lupus-prone mice and patients with systemic lupus erythematosus implicates enhanced glycolysis in lymphocytes as a driver of disease. We previously showed that the pharmacologic blockade of glycolysis reduced the production of autoantibodies without affecting antibodies induced by immunization to a foreign protein. Here we used CRISPR\/Cas9 to reduce the expression of glucose transporter GLUT1 in B cells from autoreactive AM14 Vk8R (AM14) and antigen-specific B1-8 J\u03ba (B1-8) transgenic mice, comparing intrinsic glycolytic requirements across disease-relevant contexts. Following adoptive transfer into BALB\/c recipients, Glut1 knockdown (Glut1KD) decreased the persistence of AM14 B cells, their differentiation into plasmablasts, and production of antibodies upon immunization with the PL2-3 hybridoma that activates both their B-cell receptor and endosomal TLR. In addition, PL2-3\u2013stimulated Glut1KD AM14 B cells selectively reduced their CD80 expression both in vivo and in vitro, as well as ATP production and mammalian target of rapamycin (mTOR) signaling in vitro. In contrast, Glut1KD B1-8 B cells retained persistence, plasmablast output, and nitrophenyl (NP)\u2013specific IgM production after NP-OVA immunization, with a selective reduction in the proliferation of naive B cells. Bioenergetic output was preserved despite Glut1KD in both clones stimulated with TLR7 agonist R848, but CD80 and mTOR signaling were differentially affected. Thus, GLUT1-dependent glycolysis is essential for immune complex\u2013driven autoreactive B-cell activation yet largely dispensable for antigen-specific responses, identifying metabolic checkpoints that may selectively restrain pathogenic B cells while sparing protective humoral immunity.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag092","type":"journal-article","created":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T02:58:11Z","timestamp":1778122691000},"source":"Crossref","is-referenced-by-count":2,"title":["GLUT1-mediated glucose flux constrains autoreactive but not foreign antigen-specific B-cell responses"],"prefix":"10.1093","volume":"215","author":[{"given":"Yanan","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center , San Antonio, TX,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seung Chul","family":"Choi","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center , San Antonio, TX,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2152-0959","authenticated-orcid":false,"given":"Mark J","family":"Shlomchik","sequence":"additional","affiliation":[{"name":"Program in Microbiology and Immunology, School of Medicine, University of Pittsburgh , Pittsburgh, PA,","place":["United States"]},{"name":"Department of Immunology, School of Medicine, University of Pittsburgh , Pittsburgh, PA,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurence","family":"Morel","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center , San Antonio, TX,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2026,5,7]]},"reference":[{"key":"2026090708221679700_vkag092-B1","doi-asserted-by":"crossref","first-page":"764","DOI":"10.1038\/ni0901-764","article-title":"Systemic lupus erythematosus: an autoimmune disease of B cell hyperactivity","volume":"2","author":"Lipsky","year":"2001","journal-title":"Nat Immunol"},{"key":"2026090708221679700_vkag092-B2","doi-asserted-by":"crossref","first-page":"e149095","DOI":"10.1172\/JCI149095","article-title":"Meant to B: B cells as a therapeutic target in systemic lupus erythematosus","volume":"131","author":"Atisha-Fregoso","year":"2021","journal-title":"J Clin Invest"},{"key":"2026090708221679700_vkag092-B3","doi-asserted-by":"crossref","first-page":"1841","DOI":"10.1182\/blood.2024025413","article-title":"CAR T cells in autoimmunity: game changer or stepping 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