Distinct Kinase-Independent Role of RIPK3 in CD11c⁺ Mononuclear Phagocytes in Cytokine-Induced Tissue Repair.

ABSTRACT: Receptor interacting protein kinase 3 (RIPK3) induces necroptosis, a type of regulated necrosis, through its kinase domain and receptor interacting protein (RIP) homotypic interaction motif (RHIM). In addition, RIPK3 has been shown to regulate NLRP3 inflammasome and nuclear factor κB (NF-κB) activation. However, the relative contribution of these signaling pathways to RIPK3-dependent inflammation in distinct immune effectors is unknown. To investigate these questions, we generated RIPK3-GFP reporter mice. We found that colonic CD11c⁺CD11b⁺CD14⁺ mononuclear phagocytes (MNPs) expressed the highest level of RIPK3 in the lamina propria. Consequently, deletion of the RIPK3 RHIM in CD11c⁺ cells alone was sufficient to impair dextran sodium sulfate (DSS

SUBMITTER: Moriwaki K 

PROVIDER: S-EPMC5343671 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature