Extensive works on experimental animal models demonstrate that infectious agents can break immunological tolerance to self-antigens and induce autoimmune disorders, namely systemic lupus erythematosus (SLE). The establishment of a causative link between infections and autoimmunity has been largely studied in a host of clinical studies, proving the role of infectious agents in the induction as well as in the progression or exacerbation of SLE. However, we are far from a plain understanding of microbial-host interactions in the pathogenesis of SLE. Many serological, molecular, and geoepidemiological evidences support a relationship of different environmental infectious triggers in the inception of SLE-related autoimmune phenomena with adjuvant effects. The promotion of autoimmune responses through bystander activation or epitope spreading via multiple inflammatory pathways has been confirmed in animal models. Different viruses have been implicated in SLE pathogenesis, particularly Epstein-Barr virus, but also parvovirus B19, cytomegalovirus, and retroviruses. SLE patients usually have an impaired immune response towards Epstein-Barr virus and dysregulation of viral latency period. Furthermore, the accumulation of endogenous retroviral products might trigger the production of interferon and anti-DNA antibodies. In addition, protozoan infections might even protect from autoimmune processes and rescind an ongoing B cell activation. Herein we discuss which type of infections induce, exacerbate or inhibit autoimmune disorders and analyze the principal infection-induced immunological mechanisms influencing the development of SLE.
|Editore||Elsevier Science Limited|
|Numero di pagine||12|
|Stato di pubblicazione||Pubblicato - 2015|
- Systemic lupus erythematosus