Mechanism of rituximab therapy for refractory nephritic syndrome in children

据报道，TNF-α增强中性粒细胞Nox2产生活性氧（ROS），有助于血管内皮细胞（VEC）中ICAM-1的表达，这在中性粒细胞外渗和动脉瘤形成中起关键作用。然而，这种可能性只是通过使用还原剂或抑制剂对Nox的间接研究得出的。为了得到明确的答案，我们用LCWE制作了川崎病小鼠模型，然后用Nox2-KO小鼠进行检验。检验研究清楚地表明，TNF-α诱导ICAM-1表达，直接影响VEC，而不需要中性粒细胞Nox2的ROS的帮助。

Potentiated generation of reactive oxygen spices (ROS) from neutrophil Nox2 by TNF-α was reported to contribute to ICAM-1 expression in vascular endothelial cells (VEC), which plays a key role in neutrophil extravasation and following aneurysm formation. However, this possibility was only concluded by indirect studies using reducing agents or inhibitors against Nox. In order to get a definite answer, we produced a mouse model of Kawasaki disease using LCWE, and then inspected it with Nox2-KO mice. The inspection studies clearly demonstrated that TNF-α induces ICAM-1 expression, directly affecting VEC without the aid of ROS from neutrophil Nox2.