Inverse relationship between the ratio of ICAM-1 expressing lymphocytes and serum TGF-beta 1 concentrations in acute rheumatic fever
Autoimmunity in acute rheumatic fever (ARF) is triggered by group-A beta hemolytic streptococci (GAS). Although most of the recent work has focused on the major impact of lymphocytes, the exact immunopathogenesis is still unresolved. Regulation of self-tolerance in response to GAS has been investiga...
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Published in | Journal of autoimmunity Vol. 25; no. 2; pp. 141 - 149 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
01.09.2005
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Subjects | |
Online Access | Get full text |
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Summary: | Autoimmunity in acute rheumatic fever (ARF) is triggered by group-A beta hemolytic streptococci (GAS). Although most of the recent work has focused on the major impact of lymphocytes, the exact immunopathogenesis is still unresolved. Regulation of self-tolerance in response to GAS has been investigated in various animal experiments. This study aimed to associate the ratio of lymphocytes bearing adhesion/costimulatory molecules, Bcl-2/CD95 and serum TGF-beta1 concentrations with clinical stages of ARF. Thirty-five patients were assigned according to the clinical stages. Bcl-2 expression on CD19+ and CD3+ lymphocytes was similar within patient groups and controls. CD62p expression was higher in patients with carditis. The ratio of ICAM-1 bearing lymphocytes was significantly different between patient groups and controls and was increased through acute to remission stages longitudinally. In contrast, a gradual and significant decrease in TGF-beta1 concentrations was observed longitudinally from acute to chronic stages. A positive correlation has been documented between ICAM-1+ lymphocyte ratios and Fas+ cytotoxic T cell ratios supported by a prominent increase in CD95+ T cells. These data draw our attention to the role of ICAM-1, Fas and TGF-beta1 in ARF pathogenesis through the perspective of self-tolerance in a clinical setting. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0896-8411 |
DOI: | 10.1016/j.jaut.2005.05.006 |