{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T21:09:43Z","timestamp":1789160983511,"version":"build-2803163510"},"reference-count":77,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"74","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Sci. Immunol."],"published-print":{"date-parts":[[2022,8,26]]},"abstract":"<jats:p>\n                    Tumor necrosis factor receptor\u2013associated factor 3 (TRAF3) is a central regulator of immunity. TRAF3 is often somatically mutated in B cell malignancies, but its role in human immunity is not defined. Here, in five unrelated families, we describe an immune dysregulation syndrome of recurrent bacterial infections, autoimmunity, systemic inflammation, B cell lymphoproliferation, and hypergammaglobulinemia. Affected individuals each had monoallelic mutations in\n                    <jats:italic>TRAF3<\/jats:italic>\n                    that reduced TRAF3 expression. Immunophenotyping showed that patients\u2019 B cells were dysregulated, exhibiting increased nuclear factor-\u03baB 2 activation, elevated mitochondrial respiration, and heightened inflammatory responses. Patients had mild CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cell lymphopenia, with a reduced proportion of na\u00efve T cells but increased regulatory T cells and circulating T follicular helper cells. Guided by this clinical phenotype, targeted analyses demonstrated that common genetic variants, which also reduce\n                    <jats:italic>TRAF3<\/jats:italic>\n                    expression, are associated with an increased risk of B cell malignancies, systemic lupus erythematosus, higher immunoglobulin levels, and bacterial infections in the wider population. Reduced TRAF3 conveys disease risks by driving B cell hyperactivity via intrinsic activation of multiple intracellular proinflammatory pathways and increased mitochondrial respiration, with a likely contribution from dysregulated T cell help. Thus, we define monogenic\n                    <jats:italic>TRAF3<\/jats:italic>\n                    haploinsufficiency syndrome and demonstrate how common\n                    <jats:italic>TRAF3<\/jats:italic>\n                    variants affect a range of human diseases.\n                  <\/jats:p>","DOI":"10.1126\/sciimmunol.abn3800","type":"journal-article","created":{"date-parts":[[2022,8,12]],"date-time":"2022-08-12T13:58:37Z","timestamp":1660312717000},"source":"Crossref","is-referenced-by-count":40,"title":["Immunodeficiency, autoimmunity, and increased risk of B cell malignancy in humans with\n                    <i>TRAF3<\/i>\n                    mutations"],"prefix":"10.1126","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0095-2514","authenticated-orcid":true,"given":"William","family":"Rae","sequence":"first","affiliation":[{"name":"Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of 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