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Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Immunity 2014 ; 41 (4): 567-78 Nephropedia Template TP
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The Necroptosis Adaptor RIPK3 Promotes Injury-Induced Cytokine Expression and Tissue Repair #MMPMID25367573
Immunity 2014[Oct]; 41 (4): 567-78 PMID25367573show ga
Programmed necrosis or necroptosis is an inflammatory form of cell death that critically requires the receptor interacting protein kinase 3 (RIPK3). Here we showed that RIPK3 controls a separate, necrosis-independent pathway of inflammation through regulating dendritic cells (DCs) cytokine expression. Ripk3?/? bone marrow derived dendritic cells (BMDCs) were highly defective in lipopolysaccharide (LPS)-induced expression of inflammatory cytokines. These effects were caused by impaired NF-?B subunit RelB and p50 activation and caspase 1-mediated processing of interleukin-1? (IL-1?). This DC-specific function of RIPK3 was critical for injury-induced inflammation and tissue repair in response to dextran sodium sulfate (DSS). Ripk3?/? mice exhibited an impaired axis of injury-induced IL-1?, IL-23 and IL-22 cytokine cascade, which was partially corrected by adoptive transfer of wild type DCs, but not Ripk3?/? DCs. These results reveal an unexpected function of RIPK3 in NF-?B activation, DC biology, innate inflammatory cytokine expression, and injury-induced tissue repair.