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- Francis Ka-Ming Chan
- Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, Massachusetts 01605;
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- Nivea Farias Luz
- Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, Massachusetts 01605;
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- Kenta Moriwaki
- Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, Massachusetts 01605;
抄録
<jats:p>Cell proliferation and cell death are integral elements in maintaining homeostatic balance in metazoans. Disease pathologies ensue when these processes are disturbed. A plethora of evidence indicates that malfunction of cell death can lead to inflammation, autoimmunity, or immunodeficiency. Programmed necrosis or necroptosis is a form of nonapoptotic cell death driven by the receptor interacting protein kinase 3 (RIPK3) and its substrate, mixed lineage kinase domain-like (MLKL). RIPK3 partners with its upstream adaptors RIPK1, TRIF, or DAI to signal for necroptosis in response to death receptor or Toll-like receptor stimulation, pathogen infection, or sterile cell injury. Necroptosis promotes inflammation through leakage of cellular contents from damaged plasma membranes. Intriguingly, many of the signal adaptors of necroptosis have dual functions in innate immune signaling. This unique signature illustrates the cooperative nature of necroptosis and innate inflammatory signaling pathways in managing cell and organismal stresses from pathogen infection and sterile tissue injury.</jats:p>
収録刊行物
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- Annual Review of Immunology
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Annual Review of Immunology 33 (1), 79-106, 2015-03-21
Annual Reviews