Investigation Of The Pathogenesis Of Idiopathic Thrombocytopenia Purpura In Children By Detecting Expression Of SCD40L

Background and Objectives: Idiopathic thrombocytopenia purpura (ITP) is an autoimmune bleeding disease .The pathogenesis of ITP is not completely clear yet. It is believed that immune response plays an important role in this process. Early in 1950's, people found that the destruction of platelet is mediated by anti-platelet antibodies which mainly target glycoprotein IIb/IIIa (GPIIb/IIIa). It is believed that anti-platelet antibody-opsonized platelets are eliminated through Fc-gamma receptor-mediated and complement-mediated phagocytosis by macrophages of the reticuloendothelial system (RES). In 1951, Harrington etc found that a certain humoral factor led to ITP. If we transfused it to normal individuals, it can lead to destruction of their platelets. In 1975, Dixon measured the immunoglobulin(Ig) on the surface of platelet for the first time, so platelet-associated Ig (PAIg) has been thought of as evidence of ITP.It is thought that ITP is developed with a genetic background .In addition, by the stimulation of relevant activation factors, immune function disorder was induced, especially the dysfunction of immune regulation and over-activation of T cells. Multi-colonel activation of B cells will be found and then the activated B cells produce a series of anti-platelet auto antibodies. As a result, the Ag-Abs complexes activate complements and lead to platelet damages. The immune response depends on the activation of T cells. Besides the primary signal, Ag-MHC complex, the co stimulatory signal, known as nonspecific co stimulatory...