Decreased RAGE expression in peripheral blood mononuclear cells of patients with rheumatoid arthritis.
作者： Franke S , Eidner T , Schmidt C , Wolf G , Drinda S
DOI:
关键词: Immunology 、 Rheumatoid arthritis 、 Medicine 、 RAGE (receptor) 、 Proinflammatory cytokine 、 Pathogenesis 、 Receptor 、 Peripheral blood mononuclear cell 、 Immunopathology 、 Autoimmune disease
摘要: Objective Interactions between the multiligand receptor for advanced glycation end products (RAGE) and its proinflammatory ligands (AGEs, S100/calgranulins, HMBG1, Mac-1) may contribute to inflammatory responses playing a key role in pathogenesis of chronic diseases such as rheumatoid arthritis (RA). Peripheral blood mononuclear cells (PBMCs) participate development diseases. This study investigated expression RAGE variants endogenous secretory (esRAGE), N-truncated (NtRAGE) complete (cRAGE: encoding full-length RAGE, esRAGE NtRAGE) PBMCs patients with RA comparison healthy control subjects (controls) Crohn’s disease (CD) another disease. Methods The cRAGE, NtRAGE mRNA levels from controls, CD were measured by real-time PCR. protein was determined Western blot analysis plasma ELISA. Results showed significantly decreased cRAGE (46%), (54.0%) (52%) controls (100%). For patients, also down-regulation but lower extent found 79%; esRAGE: 76%; NtRAGE: 69%). Related reduced (53%) well concentrations (70%). Conclusion isoforms intracellular mediated cell-standing lowered capability trapping circulating esRAGE.
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