New concepts in pathogenesis of primary immune thrombocytopenia

Document Type : Original Article

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1 chemical and clinical pathology , faculty of medicine , Sohag university , Sohag , Sohag

2 clinical and chemical pathology department faculty of medicine sohag university

3 clinical and chemical pathology department, medical faculty, sohag university , sohag

4 clinical and chemical pathology faculty of medicine sohag university

Abstract

Primary immune thrombocytopenia (ITP) is a common condition characterized by a low peripheral platelet count (100000/L) caused by cell-mediated and humoral-mediated destruction of the platelet. Immunological tolerance to platelet antigens is lost in these patients. The main step in the pathogenesis includes the overactivation of T-cells, particularly T-helper cells, the release of various cytokines, and the interaction of autoantibodies with platelet surface antigens, which results in platelet destruction by the immune system in the spleen. The most common PLT antigens against which autoantibodies are directed are CD41 and CD61. These antigens are occupied by autoantibodies so there is decreased detection of these antigens on the surface of platelets. PD1 is an important negative stimulatory molecule of the immune system a member of CD28/B7 family. ITP patients have considerably increased levels of PD-1 on CD4+T- cells in their peripheral blood than healthy people., indicating that the PD1 molecule plays an important role in illness etiology.
Abbreviations: ITP: Primary immune thrombocytopenia, PD1: programmed death 1.

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