Lupus nephritis (LN) is a common clinical complication in patients with systemic lupus erythematosus (SLE). A report by Mark J. Shlomchik and colleagues reveals an interplay between NADPH oxidase 2 (NOX2) and Toll-like receptor 7 (TLR7) in B cells that can modulate SLE severity, including its kidney manifestations.

The researchers propose that this protection might result from NOX2-mediated inhibition of TLR7 activity. When stimulated with a TLR7 agonist, Cybb-KO B cells had enhanced nuclear factor-κB activation compared with wild-type B cells, and in global Cybb-KO lupus mice, deleting Tlr7 in B cells had a protective effect.

狼疮性肾炎（LN）是系统性红斑狼疮（SLE）患者常见的临床并发症。 Mark J. Shlomchik 及其同事的一份报告揭示了 B 细胞中 NADPH 氧化酶 2 (NOX2) 和 Toll 样受体 7 (TLR7) 之间的相互作用，可以调节 SLE 的严重程度，包括其肾脏表现。

研究人员提出，这种保护可能是由于 NOX2 介导的 TLR7 活性抑制所致。当用 TLR7 激动剂刺激时，与野生型 B 细胞相比， Cybb -KO B 细胞的核因子-κB 激活增强，并且在整体Cybb -KO 狼疮小鼠中，删除 B 细胞中的Tlr7具有保护作用。