Shlomovitz Inbar, Zargrian Sefi, Gerlic Motti
Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Immunol Cell Biol. 2017 Feb;95(2):166-172. doi: 10.1038/icb.2016.124. Epub 2016 Dec 15.
Receptor-interacting protein kinase 3 (RIP3/RIPK3) is a multifunctional regulator of cell death and inflammation. It controls signalling downstream of the tumor necrosis factor (TNF) receptor family, DNA-dependent activator of IFN-regulatory factors (DAI) and toll-like receptors (TLRs). Today, it is also widely recognized as a component of caspase-independent cell death known as necroptosis, and cytokine production via activation of the inflammasome. Its role in inflammasome activation, in particular, make the interpretation of its role in vivo more complex. In this review, we focus on divergent roles for RIPK3 in cell death and inflammation.
受体相互作用蛋白激酶3（RIP3/RIPK3）是细胞死亡和炎症的多功能调节因子。它控制肿瘤坏死因子（TNF）受体家族、干扰素调节因子的DNA依赖性激活剂（DAI）和Toll样受体（TLR）下游的信号传导。如今，它也被广泛认为是一种不依赖半胱天冬酶的细胞死亡（即坏死性凋亡）的组成部分，以及通过激活炎性小体产生细胞因子的组成部分。特别是它在炎性小体激活中的作用，使得对其体内作用的解读更加复杂。在本综述中，我们重点关注RIPK3在细胞死亡和炎症中的不同作用。
