Figure 1.
Proposed mechanism of immune dysregulation in ITP. (A) T cells are activated upon recognition of platelet-specific antigens on the APCs and therefore induce antigen-specific expansion of B cells. The B cells in turn produce autoantibodies with specificity for glycoproteins expressed on platelets and megakaryocytes. (B) Circulating platelets bound by autoantibody are removed by Fc receptors predominantly by splenic macrophages. (C) Autoantibodies also reduce the capacity of megakaryocytes to produce platelets. Adapted with permission from Wei and Jackson.8

Proposed mechanism of immune dysregulation in ITP. (A) T cells are activated upon recognition of platelet-specific antigens on the APCs and therefore induce antigen-specific expansion of B cells. The B cells in turn produce autoantibodies with specificity for glycoproteins expressed on platelets and megakaryocytes. (B) Circulating platelets bound by autoantibody are removed by Fc receptors predominantly by splenic macrophages. (C) Autoantibodies also reduce the capacity of megakaryocytes to produce platelets. Adapted with permission from Wei and Jackson.

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