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The prevailing model holds that reduced NOX2 activity promotes SLE via defective efferocytosis, the immunologically silent clearance of apoptotic cells. Here, we describe a parallel B cell\u2013intrinsic mechanism contributing to breaks in tolerance. In keeping with an important role for B cell Toll-like receptor (TLR) pathways in lupus pathogenesis, NOX2-deficient B cells exhibit enhanced signaling downstream of endosomal TLRs, increased humoral responses to nucleic acid-containing antigens, and the propensity toward humoral autoimmunity. Mechanistically, TLR-dependent NOX2 activation promotes LC3-mediated maturation of TLR-containing endosomes, resulting in signal termination. CRISPR-mediated disruption of NCF1 confirmed a direct role for NOX2 in regulating endosomal TLR signaling in primary human B cells. Together, these data highlight a new B cell\u2013specific mechanism contributing to autoimmune risk in NCF1 and NCF2 variant carriers.<\/jats:p>","DOI":"10.1084\/jem.20230774","type":"journal-article","created":{"date-parts":[[2024,1,17]],"date-time":"2024-01-17T02:21:08Z","timestamp":1705458068000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":26,"title":["NADPH oxidase exerts a B cell\u2013intrinsic contribution to lupus risk by modulating endosomal TLR signals"],"prefix":"10.1084","volume":"221","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9067-1195","authenticated-orcid":true,"given":"Shuozhi","family":"Liu","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01njes783","id-type":"ROR","asserted-by":"publisher"}],"name":"Seattle Children\u2019s Research Institute 1 , Seattle, WA, 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