The role of T cells and myeloid‐derived suppressor cells in refractory immune thrombocytopenia

Abstract

SummaryImmune thrombocytopenia (ITP) is characterized by a dysregulated immune response against platelets, affecting both their destruction and production. A role for an abnormal T‐cell compartment has been established in ITP pathogenesis and treatments that increase platelet counts in patients with ITP have shown improvements in T‐cell profiles. On the other hand, patients who were refractory to treatment appear to retain the T‐cell abnormalities as before. Myeloid‐derived suppressive cells (MDSCs) are also emerging as key contributors to the immune pathology of ITP and response to treatment. In this review, we will discuss how various treatments affect the T‐cell and MDSC compartments in ITP. The review will focus on studies that have examined the underlying mechanisms and/or genetic basis responsible for refractoriness to a given treatment and highlight remaining challenges in identifying factors and mechanisms to predict response to treatment.

The miR-641-STIM1 and SATB1 axes play important roles in the regulation of the Th17/Treg balance in ITP

“…The destruction of platelets in ITP occurs primarily through two mechanisms: antibody-mediated clearance by the spleen and immune-mediated damage to megakaryocytes. The currently known T cells dysfunctions of ITP includes T-cell toxicity 1 , abnormal regulatory T cells [2][3][4] , an imbalance in helper T cells 5,6 , abnormal T-cell responses 7,8 . A growing body of research suggests that the Treg/Th17 balance plays a key role in the development of ITP 4,[9][10][11] .…”