Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8736388 | Autoimmunity Reviews | 2018 | 42 Pages |
Abstract
Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are two phenotypically distincts inflammatory systemic diseases. However, SLE and SSc share pathogenic features such as interferon signature, loss of tolerance against self-nuclear antigens and increased tissue damage such as fibrosis. Recently, platelets have emerged as a major actor in immunity including auto-immune diseases. Both SLE and SSc are characterized by strong platelet system activation, which is likely to be both the witness and culprit in their pathogenesis. Platelet activation pathways are multiple and sometimes redundant. They include immune complexes, Toll-like receptors activation, antiphospholipid antibodies and ischemia-reperfusion associated with Raynaud phenomenon. Once activated, platelet promote immune dysregulation by priming interferon production by immune cells, providing CD40L supporting B lymphocyte functions and providing a source of autoantigens. Platelets are actively implicated in SLE and SSc end-organ damage such as cardiovascular and renal disease and in the promotion of tissue fibrosis. Finally, after understanding the main pathogenic implications of platelet activation in both diseases, we discuss potential therapeutics targeting platelets.
Keywords
ICAMBTGvWFMMP-9ET-1TLRECMRAGETIMP-1MCP-1MPVTxA2HMGB-1HCQPSGL-1TFHTSLPPMPPGI2COXDAMPAPLSSCMitochondrial DNAsystemic sclerosisHITdamage-associated molecular patternsendothelin-1cardiovascular diseaseHeparin-induced thrombocytopeniaThromboxane A2neutrophil extracellular trapToll-like receptorNETAuto-immunitymtDNAMicroparticleMicroparticlesCVDRaynaud phenomenonEndothelial cellsantiphospholipidVon Willebrand factorVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)Thymic stromal lymphopoietinSystemic lupus erythematosusSLEExtracellular matrixMatrix metalloprotease-9mean platelet volumeimmune complexintercellular adhesion moleculelupus nephritishydroxychloroquinemonocyte chemoattractant protein-1prostacyclinPlateletsplatelet-derived microparticlesT follicular helperHigh-mobility group Box-1
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Authors
Marc Scherlinger, Vivien Guillotin, Marie-Elise Truchetet, Cécile Contin-Bordes, Vanja Sisirak, Pierre Duffau, Estibaliz Lazaro, Christophe Richez, Patrick Blanco,