Proteomic and immunohistochemistry analyses revealed erratic GPIIB expression by the tumor cells, suggesting possible antigenic mimicry chronically stimulating the immune system and leading to this patient's refractory ITP.
These changes are thought to affect markers of haematopoietic stem cells, such as CD41 and CD61, and differentiation of megakaryocytes, ultimately decreasing the function and quantity of platelets and leading to the onset of ITP.
The Levels of T Lymphocyte Subsets in Immune Thrombocytopenia Associated with Anti-GPIIb/IIIa- and/or Anti-GPIbα-Mediated Responses Are Differentially Sensitive to Dexamethasone.
However, the differences in correlations between the numbers of epitopes in AA and ITP patients suggest that the epitopes of GPIIb/IIIa are altered in these diseases.
We found that platelet-associated CD154 is competent to induce the CD40-dependent proliferation of B lymphocytes, and we observed an in vitro CD154-dependent production of antibodies to the GPIIb/IIIa complex (integrin alphaIIbbeta3) when platelets and peripheral blood B lymphocytes from ITP patients with circulating anti-GPIIb/IIIa antibody were cultured together.
In this study, we detected autoantibodies to platelet glycoproteins GPIIb/IIIa and GPIb/IX on platelets and in plasma in a patient with immune thrombocytopenia associated with Epstein-Barr virus-related infectious mononucleosis.