PI3Kδ and PI3Kγ:: partners in crime in inflammation in rheumatoid arthritis and beyond?

被引：351

作者：

Rommel, Christian ^{[1
]}

Camps, Montserrat ^{[1
]}

Ji, Hong ^{[1
]}

机构：

[1] Merck Serono Int SA, CH-1211 Geneva, Switzerland

来源：

NATURE REVIEWS IMMUNOLOGY | 2007年 / 7卷 / 03期

关键词：

D O I：

10.1038/nri2036

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Dysregulated signal transduction in innate and adaptive immune cells is known to be associated with the development of various autoimmune and inflammatory diseases. Consequently, targeting intracellular signalling of the pro-inflammatory cytokine network heralds hope for the next generation of anti-inflammatory drugs. Phosphoinositide 3-kinases (PI3Ks) generate lipid-based second messengers that control an array of intracellular signalling pathways that are known to have important roles in leukocytes. In light of the recent progress in the development of selective PI3K inhibitors, and the beneficial effects of these inhibitors in models of acute and chronic inflammatory disorders, we discuss the therapeutic potential of blocking PI3K isoforms for the treatment of rheumatoid arthritis and other immune-mediated diseases.

引用

页码：191 / 201

页数：11

共 127 条

[41] Hypoglycaemia, liver necrosis and perinatal death in mice lacking all isoforms of phosphoinositide 3-kinase p85α [J].