Mechanism of rituximab therapy for refractory nephritic syndrome in children

肿瘤坏死因子-α促进中性粒细胞产生活性氧香料(ROS)有助于血管内皮细胞ICAM-1的表达，而ICAM-1在中性粒细胞外渗和随后的动脉瘤形成中起关键作用。然而，这种可能性只有通过使用还原剂或抑制剂对抗NOx的间接研究才能得出结论。为了得到一个确切的答案，我们用LCWE制作了川崎病的小鼠模型，然后用NOX2-KO小鼠进行了检验。检查研究清楚地表明，肿瘤坏死因子-α诱导细胞间黏附分子-1的表达，直接影响血管内皮细胞，而不需要中性粒细胞NOX2产生的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.