Abstract
Exogenous and endogenous environmental exposures and particularly infections may participate in the breakage of tolerance and the induction of autoimmunity in rheumatic diseases. Response to infections apparently occurs years before clinical manifestations and features of autoimmunity, such as autoantibodies, are detected years before clinical manifestations in autoimmune rheumatic diseases. In this review, we summarize the current evidence for a potential causal link between infectious agents and rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjogren’s syndrome and ANCA-associated vasculitis.
Highlights
Abbreviations ab AntibodyAnti-citrullinated peptide antibodies (ACPAs) Anti-citrullinated peptide antibodycitrullinated aenolase peptide-1 (CEP-1) Citrullinated a-enolase peptide-1 collagen-induced arthritis (CIA)Collagen-induced arthritis EBVEpstein-Barr virusEBNA-1 EBV nuclear antigen-1 ELSEctopic lymphoid follicle-like structuresgraft-versus-host disease (GVHD) Graft-versus-host disease human cytomegalovirus (hCMV) Human cytomegalovirus
We summarize the current evidence for a potential causal link between infectious agents and rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjogren’s syndrome and ANCA-associated vasculitis
P. gingivalis DNA can induce IL-1, IL-6 and TNFa production in a monocytic cell line through TLR9 [40]. These findings suggest that bacterial persistence in the joints may contribute to the synovial inflammation in rheumatoid arthritis (RA)
Summary
Infectious agents have long been suspected as initiating agents (etiology) of rheumatic diseases. Epidemiological and family studies have shown that environmental factors play a significant role in the development of rheumatic diseases [1]. This is exemplified by the low concordance rate of RA in monozygotic twins but higher than that in dizygotic twins. An immune response to an infectious agent may result in an autoimmune disease by molecular mimicry, epitope spreading, bystander activation or pathogen persistence [3, 4].
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