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The adaptor protein TRAF3 regulates B cell survival, activation, and differentiation by restraining signaling through Toll-like receptors, tumor necrosis factor (TNF) receptor superfamily members, and the B cell antigen receptor\u2014pathways linked to autoimmunity and lymphoma. Mice lacking TRAF3 in B cells (B-Traf3\u2212\/\u2212) develop both autoimmunity and B cell malignancies. TRAF3 negatively regulates activation of spleen tyrosine kinase (Syk), which is involved in multiple B cell signaling pathways. B-Traf3\u2212\/\u2212 mice treated with the Food and Drug Administration (FDA)-approved Syk inhibitor Fostamatinib, exhibited reduction in autoantibodies, gland inflammation, and expansion of autoimmune-associated B cell populations. Fostamatinib also corrected enhanced pro-survival proteins and aberrant B cell survival in Traf3\u2212\/\u2212 B cells, without inhibiting humoral responses to immunization. These findings identify elevated Syk activation as a key driver of B cell dysfunction and autoimmunity in B-Traf3\u2212\/\u2212 mice, suggesting therapeutic potential for Syk inhibitors in conditions linked to decreased B cell TRAF3 levels.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag049","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T03:24:19Z","timestamp":1777001059000},"source":"Crossref","is-referenced-by-count":0,"title":["Syk inhibition limits autoimmunity and abnormal B cell phenotype and function in mice with B cell-specific TRAF3 deficiency"],"prefix":"10.1093","volume":"215","author":[{"given":"Emma L","family":"Hornick","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology and Holden Comprehensive Cancer Center, University of Iowa , Iowa City, IA,","place":["United 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