The immunopathogenesis of immune thrombocytopenia: T cells still take center-stage

PURPOSE OF REVIEW: Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder in which T and B cells recognize platelet antigens and initiate antiplatelet destructive mechanisms such as peripheral Fc receptor-mediated phagocytosis in the spleen or megakaryocyte destruction/inhibition within the bone marrow. The purpose of this review is to report on the ITP pathophysiology literature published from January 2011 to early in 2012.

RECENT FINDINGS: The underlying stimulus of platelet autoimmunity is not known; however, in 2011, as in previous years, there has been a significant contribution of published studies addressing the pathophysiology of ITP. At least half of the 2011 ITP pathophysiology literature was associated with T-cell dysregulation particularly with respect to T-helper 17 cell and related cytokine and genetic studies. There were also studies related to B-cell responses, human spleen cells and the potential role of oxidative stress in ITP. With respect to therapeutic research, the mechanisms of action of intravenous gammaglobulin relating to Fc inhibitory receptors and sialylation have been challenged.

SUMMARY: The overall landscape of pathophysiological research into ITP still is overwhelmed by studies on abnormal T-cell responses and these studies are beginning to clarify the underlying immune mechanisms that are responsible for the disorder.