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

M Blank, Y Shoenfeld, A Perl

Journal: Lupus 2010;18(13):1136-43

PMID: 19880559

Abstract

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.

Address: Center for Autoimmune Diseases, an Department of Medicine B, Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer, Israel.

DOI: 10.1177/0961203309345728

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MeSH Terms: Amino Acid Sequence, Antigens, Viral, Autoantigens, Endogenous Retroviruses, Environment, Epigenesis, Genetic, Epitopes, Gene Expression Regulation, Viral, Genome, Human, Herpesvirus 4, Human, Humans, Immune System, Lupus Erythematosus, Systemic, Molecular Mimicry, Molecular Sequence Data, Torque teno virus