The anti-snRNP autoimmune response in rheumatic diseases is polyclonal and likely antigen-driven.
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Antigen-driven polyclonal anti-snRNP responses warrant epitope mapping in rheumatic diseases; animal data leave open human translation.
Autoantibodies against small nuclear ribonucleoproteins (snRNP) are common in systemic lupus erythematosus and related disorders. The 3 categories, anti-(U1)RNP, anti-(U1, U2)RNP, and anti-Sm, all contain a common antibody specificity directed against the U1 snRNP-associated A protein. To determine the specificity of anti-U1 snRNP A protein antibodies for various antigenic sites, we tested 26 different anti-snRNP-positive sera for reactivity with fragments of the U1 snRNP A protein, which was produced using recombinant DNA technology. Several different fragments were shown to contain autoimmune-reactive epitopes, which indicates that the antibody response against the U1 snRNP A protein is polyclonal. Antibodies against a discontinuous or conformational epitope were found in most of the sera tested, regardless of whether they were classified as anti-(U1)RNP, anti-Sm, or anti-(U1, U2) RNP. These results strongly support the hypothesis that the anti-snRNP autoimmune response is antigen driven.
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Habets et al. (1990) studied this question.
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