DOI: 10.1016/J.BERH.2019.101473
关键词: Dysbiosis 、 Rheumatoid arthritis 、 Connective tissue disease 、 Medicine 、 Autoimmunity 、 Scleroderma 、 Microbiome 、 Rheumatic fever 、 Immune system 、 Immunology
摘要: Abstract Microbial contributions to the immunopathogenesis of autoimmune rheumatic diseases have been studied since advent germ theory in 19th century. With exception Group A Streptococcus fever, early studies failed establish causal relationships between specific pathobionts and disease. Today, systemic are thought result from a complex interplay environmental factors, individual genetic risk, stochastic events. Interactions microbiota immune system shown promote sustain chronic inflammation autoimmunity. In mechanistic studies, microbe-immune cell interactions implicated initiation diseases, e.g., through posttranslational modification autoantigens rheumatoid arthritis or neutrophil death cross-reactivity with commensal orthologs lupus erythematosus. parallel, modern molecular techniques catalyzed study microbiome diseases. Here, I review current insights gained into skin, oral, gut, lung, vascular connective tissue vasculitis. Mechanism relevant development propagation autoimmunity will be discussed whenever explored. While on disease almost invariably abnormal structure (dysbiosis), substantial variability microbial composition makes generalization difficult. Moreover, an etiopathogenic role cannot inferred by association alone. Integrating descriptive communities hypothesis-driven research informed important elucidating targetable mechanisms preclinical established