MAJOR TRYPANOSOMA-CRUZI ANTIGENIC DETERMINANT IN CHAGAS HEART-DISEASE SHARES HOMOLOGY WITH THE SYSTEMIC LUPUS-ERYTHEMATOSUS RIBOSOMAL P-PROTEIN EPITOPE
MAJOR TRYPANOSOMA-CRUZI ANTIGENIC DETERMINANT IN CHAGAS HEART-DISEASE SHARES HOMOLOGY WITH THE SYSTEMIC LUPUS-ERYTHEMATOSUS RIBOSOMAL P-PROTEIN EPITOPE
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DOI:
10.1128/jcm.28.6.1219-1224.1990
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发表时间:
1990-06-01
影响因子:
9.4
通讯作者:
LEVIN, MJ
中科院分区:
文献类型:
--
作者:
MESRI, EA;LEVITUS, G;LEVIN, MJ
A Trypanosoma cruzi .lambda.gt11 cDNA clone, JL5, expressed a recombinant protein which was found to react predominantly with chronic Chagas'' heart disease sera. The cloned 35-residue-long peptide was identified as the carboxyl-terminal portion of a T. cruzi ribosomal P protein. The JL5 13 carboxyl-terminal residues shared a high degree of homology with the systemic lupus erythematosus (SLE) ribosomal P protein epitope. Synthetic peptides comprising the 13 (R-13), 10 (R-10), and 7 (R-7) carboxyl-terminal residues of the JL5 protein were used to study, by enzyme-linked immunosorbent assay, the specificity of the Chagas'' disease anti-JL5 and SLE anti-P antibodies. The R-13 peptide defined a linear antigenic determinant of the JL5 recombinant protein. As was proved for JL5, R-13 defined antibody specificities which were significantly increased in chronic Chagas'' heart disease patients. Only SLE anti-P positive sera were found to react with JL5 and R-13. Fine epitope mapping showed that Chagas'' disease anti-JL5 and SLE anti-P antibodies define similar epitopes within the R-13 peptide. The binding of the SLE sera to JL5 was completely blocked by the R-13 peptide, indicating that the shared specificity between anti-JL5 and anti-P autoantibodies was exclusively limited to the conserved linear epitope(s) within the R-13 peptide. The prevalence of high anti-R-13 antibody titers in Chagas'' heart disease patients supports the hypothesis that postulates the existence of autoimmune disorders in Chagas'' heart disease.