Infections and Systemic Lupus Erythematosus: Binding or Sparring Partners?

Extensive work on experimental animal models clearly demonstrates that infectious agents can break immunological tolerance to self-antigens and induce autoimmune disorders, mainly systemic lupus erythematosus (SLE). The establishment of a causative link between infections and autoimmunity has been l...

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Bibliographic Details
Published in:International journal of molecular sciences 2015-07, Vol.16 (8), p.17331-17343
Main Authors: Rigante, Donato, Esposito, Susanna
Format: Article
Language:English
Subjects:
Animals
Antigens
Autoimmunity
Epstein-Barr virus
Herpesviridae
Host-Pathogen Interactions - immunology
Humans
Immune system
Lupus
Lupus Erythematosus, Systemic - etiology
Lupus Erythematosus, Systemic - immunology
Lupus Erythematosus, Systemic - virology
Parvoviridae
Retroviridae
Review
Virus Diseases - complications
Virus Diseases - immunology
Viruses
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Summary:Extensive work on experimental animal models clearly demonstrates that infectious agents can break immunological tolerance to self-antigens and induce autoimmune disorders, mainly 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. Much serological, molecular and geoepidemiological evidence supports the 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 the 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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms160817331