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Chronic idiopathic thrombocytopenic purpura (ITP): molecular mechanisms and implications for therapy

Published online by Cambridge University Press:  12 November 2004

Per-Ola Andersson
Affiliation:
Section of Haematology and Coagulation, Department of Internal Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden.
Hans Wadenvik
Affiliation:
Section of Haematology and Coagulation, Department of Internal Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden.

Abstract

Chronic idiopathic thrombocytopenic purpura (ITP) is an immune-mediated disorder in which platelets are prematurely destroyed in the reticuloendothelial system by platelet autoantibodies. However, it is becoming clear that the pivotal process of the humoral immune response in the pathogenesis of the disorder is a complex interaction between antigen-presenting cells, T cells and B cells. Furthermore, it is increasingly evident that regulatory T cells play an important role and that T-cell-mediated cytotoxicity contributes to the destruction of platelets in ITP. Different new approaches to immunotherapy in chronic ITP have been explored, including use of anti-CD20, anti-CD154 and anti-CD52 antibodies. So far, these therapies have been antigen-nonspecific and the risk of general immunosuppression is a concern. Thus, improving our understanding of the interaction and relative contribution of humoral and cell-mediated mechanisms is essential for developing antigen-specific immunotherapies for the treatment of this disorder. This review aims to elucidate the current status of knowledge of the cellular and humoral immune components of chronic ITP, together with the implications of this knowledge for therapy.

Type
Review Article
Copyright
© Cambridge University Press 2004

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