ABSTRACT
Immune (autoimmune) thrombocytopenic purpura (ITP) is a syndrome characterized by persistant thrombocytopenia, which is caused by autoantibodies binding to platelet membrane antigens and mediating the destruction of platelets in the reticuloendothelial system, particularly the spleen and liver. It has been generally believed that the triad of ITP are thrombocytopenia, normal or increased megakariocytosis in the bone marrow, and decreased platelet lifespan (PLS). Although a great deal of progress has been made in understanding the nature of platelet-specific autoantigens, the pathogenicity of antibodies (Abs) and their roles in the etiology of ITP remain unclear. The discovery of a spontaneous animal model for ITP has, therefore, been long awaited. We have found the (NZW×BXSB)F1 (W/B F1) mouse to be such a model (1), although the W/B F1 mouse is not an animal model for pure ITP, since the mice develop SLE and other autoimmune diseases. However, this mouse is a useful animal model for analyzing the etiopathogenesis of ITP.
