Platelet autoantibodies

Immune response against platelet surface antigens results in antiplatelet antibodies production, which is the basis for most immune thrombocytopenias: idiopathic, drug-induced, post-transfusion and neonatal alloimmune thrombocytopenia (NAIT), such as refractoriness to random donor platelets. Immune thrombocytopenic purpura (ITP) is a common acquired autoimmune disorder defined by a low platelet count secondary to accelerated platelet removal by antiplatelet antibodies. ITP can be classified based on the absence or presence of other diseases (primary or secondary), patient age (adult or childhood), and duration (acute or chronic). The antiplatelet antibodies are mainly IgG mostly against glycoproteins (GP) IIb/IIIa and GPIb/IX complexes. The autoantibodies' production is under the control of T helper cells and their cytokines. Abnormal T cell responses drive the differentiation of auto-reactive B cell clones and autoantibody secretion. Antibody-coated platelets bind antigen-presenting cells through Fc-receptors in the spleen, but also by the mononuclear phagocyte system. The diagnosis is based on clinical and serological findings. A variety of antigen-specific assays, such as fluorescence flow cytometry, immunoblot, immunoprecipitation, immunobead, and monoclonal antibody-specific immobilization of antibodies (MAIPA) as well as molecular genotyping of platelet antigen polymorphisms are useful. Involvement of human leukocyte antigens (HLA) class I and II was reported in ITP and NAIT development, explains the hereditary tendency of the immune diseases in some of the cases.