ArticleJournal of biomedical science2026
NOX2 deficiency exacerbates lupus nephritis through activation of NLRP3 inflammasome in neutrophils.
Article in Journal of biomedical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE) associated with significant morbidity. Although reduced production of reactive oxygen species (ROS) by neutrophils correlates with severe SLE, the specific mechanisms linking ROS deficiency to heightened renal inflammation remain unknown. We aimed to elucidate the role of NOX2-derived ROS in LN pathogenesis and identify potential therapeutic targets.
methodsWe conducted an in vivo study using a pristane-induced lupus model in Ncf1
resultsNOX2 deficiency exacerbated LN severity compared to wild-type controls, demonstrated by increased serum anti-dsDNA antibody titers and worsened LN scores. Through scRNA-seq, we identified a distinct, activated neutrophil subset in Ncf1
conclusionOur results showed that NOX2 deficiency was associated with the expansion of a highly inflammatory renal neutrophil subset that may contribute to aggravated renal inflammation. These findings suggest that NOX2 functions as a negative regulator of the NLRP3 inflammasome and IL-1β blockade represents a promising precision therapeutic strategy for patients with LN who exhibit impaired ROS production.
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