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Title: CpG DNA: A pathogenic factor in systemic lupus erythematosus?

Journal Article · · Journal of Clinical Immunology
DOI:https://doi.org/10.1007/BF01541318· OSTI ID:182167
 [1]
  1. Univ. of Iowa College of Medicine, Iowa City, IA (United States)

Systemic lupus erythematosus (SLE) is a multifactorial disease of unknown etiology. Characteristic features of SLE include (1) polyclonal B cell activation, (2) overexpression of the immune stimulatory cytokine interleukin-6 (IL-6), (3) defective tolerance to self antigens, and (4) production of anti-DNA antibodies (Ab). Bacterial infection has been suspected as a triggering factor for lupus. Bacterial DNA differs from vertebrate DNA in the frequency and methylation of CpG dinucleotides. These CpG motifs in bacterial DNA induce a variety of immune effects, including (1) polyclonal activation of murine and human B cells, (2) IL-6 secretion, and (3) resistance to apoptosis, thereby potentially allowing the survival of autoreactive cells. These results suggest that microbial DNA could therefore be a pathogenic factor in SLE. SLE patients have elevated levels of circulating plasma DNA which is reportedly enriched in hypomethylated CpGs. Genomic DNA is also hypomethylated in SLE. The purpose of this review is to summarize the immune effects of CpG motifs and to present the evidence for their possible involvement in the pathogenesis of SLE. 77 refs.

Sponsoring Organization:
USDOE
OSTI ID:
182167
Journal Information:
Journal of Clinical Immunology, Vol. 15, Issue 6; Other Information: PBD: Nov 1995
Country of Publication:
United States
Language:
English

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