The Role of Cell Death in the Pathogenesis of SLE: Is Pyroptosis the Missing Link?
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Summary
While the role of pyroptosis in SLE is hypothetical at this time, further analysis of this death form should provide new insights into lupus pathogenesis and provide the missing link between infection and the initiation of l upus by products of dead and dying cells.
- Type
- review
- Published
- 2015-09-01
- Cited by
- 71
- References
- 52
- Access
- Open access
- OpenAlex
- https://openalex.org/W1799821384
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:33650311
Keywords
Pyroptosis, Inflammasome, HMGB1, Systemic lupus erythematosus, Inflammation
References
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- Recent Developments in the Role of High-Mobility Group Box 1 in Systemic Lupus Erythematosus
- The Role of HMGB1 in the Pathogenesis of Inflammatory and Autoimmune Diseases
- Neutrophil extracellular traps (NETs): Double-edged swords of innate immunity
- Caspase-1 induced pyroptotic cell death
- P2X7 Blockade Attenuates Murine Lupus Nephritis by Inhibiting Activation of the NLRP3/ASC/Caspase 1 Pathway
- The glycine-alanine repeating region is the major epitope of the Epstein-Barr nuclear antigen-1 (EBNA-1).
- Association of interleukin-18 and systemic lupus erythematosus
- Structures of The HIN Domain:DNA Complexes Reveal Ligand Binding and Activation Mechanisms of The AIM2 Inflammasome and IFI16 Receptor
- New mechanisms of NOD-like receptor-associated inflammasome activation
- HMGB1: A multifunctional alarmin driving autoimmune and inflammatory disease
- The role of defective clearance of apoptotic cells in systemic autoimmunity
- Macrophage endocytosis of high-mobility group box 1 triggers pyroptosis
- The Complex Role of DNA, Histones and HMGB1 in the Pathogenesis of SLE
- Decoding cell death signals in inflammation and immunity.
- From the authors
- Constitutive Interferon-Inducible Protein 16-Inflammasome Activation during Epstein-Barr Virus Latency I, II, and III in B and Epithelial Cells
- Pyroptotic cell death defends against intracellular pathogens
Cited by
- The Absent in Melanoma 2-Like Receptor IFN-Inducible Protein 16 as an Inflammasome Regulator in Systemic Lupus Erythematosus: The Dark Side of Sensing Microbes
- Connective tissue diseases: Nucleosomes and systemic sclerosis
- The Interplay of Lipoproteins and Innate Immune Responses in Systemic Lupus Erythematosus and its Role in Premature Cardiovascular Disease.
- Systemic lupus erythematosus: still a challenge for physicians
- Progress in understanding the diagnostic and pathogenic role of autoantibodies associated with systemic sclerosis
- Cell death in the pathogenesis of systemic lupus erythematosus and lupus nephritis
- Silica-Triggered Autoimmunity in Lupus-Prone Mice Blocked by Docosahexaenoic Acid Consumption
- Laboratory testing for the diagnosis, evaluation, and management of systemic lupus erythematosus: Still more questions for the next generations: A Tribute and Thanks and in Memory of my mentor: Henry G. Kunkel.
- Purinergic signalling in autoimmunity: A role for the P2X7R in systemic lupus erythematosus?
- The crossroads between cancer immunity and autoimmunity: antibodies to self antigens.
- Distinct proteome pathology of circulating microparticles in systemic lupus erythematosus
- B Cell Extrinsic Myd88 and Fcer1g Negatively Regulate Autoreactive and Normal B cell Immune Responses
- HMGB1 Protein: A Therapeutic Target Inside and Outside the Cell.
- Therapy with belimumab may suppress the response of peripheral blood mononuclear cells to apoptotic cells
- Origin and Consequences of Necroinflammation.
- The Neutrophil’s Choice: Phagocytose vs Make Neutrophil Extracellular Traps
- High-mobility group box 1 protein (HMGB1) operates as an alarmin outside as well as inside cells.
- Constitutive interferon signaling maintains critical threshold of MLKL expression to license necroptosis
- 29-kDa FN-f inhibited autophagy through modulating localization of HMGB1 in human articular chondrocytes
- Calpain drives pyroptotic vimentin cleavage, intermediate filament loss, and cell rupture that mediates immunostimulation
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