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Lupus
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Cross-talk of the environment with the host genome and the immune system through endogenous retroviruses in systemic lupus erythematosus

M. Blank

Center for Autoimmune Diseases, an Department of Medicine 'B', Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer, Israel, shoenfel{at}post.tau.ac.il

Y. Shoenfeld

Center for Autoimmune Diseases, an Department of Medicine 'B', Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer, Israel, Incumbent of the Laura Schwarz-Kip Chair for Research of Autoimmune Diseases, Tel-Aviv University, Israel

A. Perl

Division of Rheumatology, Department of Medicine, State University of New York Upstate Medical University, Syracuse, NY, USA

Environmental factors are capable of triggering the expression of human endogenous retroviruses and induce an autoimmune response. Infection can promote the expression of human endogenous retroviruses by molecular mimicry or by functional mimicry. There are additional mechanisms which may control the expression of human endogenous retroviruses, such as epigenetic status of the genome (hypomethylation, histone deacetylation). Ultraviolet exposure, chemicals/drugs, injury/stress, hormones, all as a single cause or in a concert, may modulate the involvement of human endogenous retroviruses in pathogenic processes. In the current review we summarize the current knowledge on infections, molecular mimicry, cross-reactivity and epigenetics contribution for trigger human endogenous retroviruses expression and pathogenesis in lupus patients. Lupus (2009) 18, 1136—1143.

Key Words: autoimmunity • systemic lupus erythematosus • endogenous retrovirus • molecular mimicry

Lupus, Vol. 18, No. 13, 1136-1143 (2009)
DOI: 10.1177/0961203309345728
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