[Progress of studies on molecular immunology of human platelets]

In autoimmune thrombocytopenic purpura (AITP) specific autoantibodies bind platelet GP via their Fab fragments. Both splenic CD5+ B and CD5- B cells produce platelet glycoprotein-specific antibodies. There is limited number of antigenic determinants, and the GP-specific autoantibodies are derived from a restricted number of B-cell clones in chronic AITP. Blocking co-stimulatory signals could induce platelet-specific T cell anergy. MMF could be used as a second line agent for the treatment of steroid-resistant AITP. Detection of plasma thrombopoietin levels play an important role in the differentiation of thrombocytopenic states caused by platelet destruction or due to bone marrow hypoplasia. Endogenous TPO level is also important on the differential diagnosis of ET and RT. Quinine- or heparin-dependent antibodies could induce thrombocytopenia. PCR-SSP is useful for the genotyping of the platelet-specific alloantigen HPA. Biotinylated platelets have an impaired response to agonists as evidenced by in vitro platelet aggregation tests.