The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
The Necroptosis Adaptor RIPK3 Promotes Injury-Induced Cytokine Expression and Tissue Repair
Open accessAbstract
Summary 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-κB subunit RelB and p50 activation and caspase 1-mediated processing of interleukin-1β (IL-1β). 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-1β, 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-κB activation, DC biology, innate inflammatory cytokine expression, and injury-induced tissue repair.
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Metadata
- Authors
- Moriwaki, K., Balaji, S., McQuade, T., Malhotra, N., Kang, J., & Chan, F. K.-M.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2014-10
- Volume
- 41
- Issue
- 4
- Pages
- 567-578
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2077684186
- Cited by
- 254
- References
- 14
- FWCI
- 8.27
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Moriwaki, K., Balaji, S., McQuade, T., Malhotra, N., Kang, J., & Chan, F. K.-M. (2014). The Necroptosis Adaptor RIPK3 Promotes Injury-Induced Cytokine Expression and Tissue Repair. Immunity. https://doi.org/10.1016/j.immuni.2014.09.016
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