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Curr Opin Rheumatol. 1997 Sep;9(5):387-92.

Autoantibodies in systemic lupus erythematosus.

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  • 1Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, México DF, México.

Abstract

Research on pathogenic and nonpathogenic anti-DNA antibodies has shown that the charge and affinity for double-stranded DNA may not be adequate predictors of their pathogenicity. In turn, anti-DNA-induced renal damage could be caused by differences in fine specificities. Penetration of anti-double-stranded DNA monoclonal antibodies into live cells appears to require DNA or a DNA-like membrane receptor. Anti-U1 ribonucleoproteins penetrate live cells and induce apoptosis. HLA-DRB1*1501 or HLA-DRB1*1503, DQA1*0102, and DQB1*0602 haplotypes were increased in patients with systemic lupus erythematosus with anti-ribosomal protein P (anti-P) antibodies, particularly in whites, blacks, and Mexican-Americans. Anti-Ro/Sjögren's syndrome antigen A antibodies had a strong predictive diagnostic value for systemic lupus erythematosus among patients positive for antinuclear antibodies and negative for double-stranded DNA but had no utility among those positive for both antinuclear antibodies and anti-DNA antibodies. True antiphospholipid murine monoclonal antibodies display an unusual number of cationic residues in the H-chain CD3 region, whereas anti-beta 2-glycoprotein-I monoclonal antibodies lack them. The association of IgG anti-beta 2-glycoprotein-I with a history of thrombosis in systemic lupus erythematosus has been largely confirmed. Apoptotic thymocytes bind antiphospholipid antibodies in a beta 2-glycoprotein-I-dependent manner and may constitute a source of immunogen in autoimmune disease.

PMID:
9309193
[PubMed - indexed for MEDLINE]
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