الفهرس 
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Abstract
Primary immune thrombocytopenia (ITP) is an immune-mediated bleeding disorder in which platelets are opsonized by glucoprotein (GP)-specific autoantibodies and prematurely cleared by phagocytic cells in the reticuloendothelial system.
The pathogenetic mechanisms of ITP remain unclear. Many pathways may be involved in the pathogenesis of ITP such as failure of immune tolerance, autoreactive B and T cells, and abnormality of cytokines.
The autoantibodies produced by autoreactive B cells against self-antigens are considered to play a crucial role. In addition to accelerated platelet destruction, autoantibodies binding to megakaryocyte membranes could interfere with megakaryocyte maturation, thus resulting in decreased platelet production.
Therefore, ITP is generally considered as a prototype of B-cell-mediated autoimmune disorder, although cytotoxic T-lymphocyte (CTL)-mediated lysis of autologous platelets has been established as an alternative mechanism for platelet destruction.
Based on the pivotal roles of B-cell in ITP, B-cell–depleting therapy with rituximab has been used as a second-line therapy for the treatment of chronic ITP for a decade with relatively high efficacy and safety.
Thus, it is reasonable to postulate that B-cell–targeted agents have therapeutic potential for the management of ITP. BAFF plays a crucial role in B-cell development, survival, and production of Igs. However, excess BAFF results in the rescue of self-reactive B cells from anergy and the rescue of autoreactive T cells from the suppressing effect of dendritic cells, thus implicating a role in the development of autoimmunity.