Immune thrombocytopenia: a review on the pathogenetic role of immune cells

Immune thrombocytopenia [ITP] is a common bleeding disorder with an isolated platelet count of less than 100 × 10⁹/L.

Relevant literature from 2003 to 2022 was retrieved and reviewed from the Google Scholar search engine and PubMed database. Antibodies produced by autoreactive B lymphocytes and the phagocytic function of macrophages are considered the most critical factors in platelet destruction. Also, macrophages present the antigen to T lymphocytes and activate them. Follicular helper T-cells [TFH] play a role in stimulating, differentiating, and activating autoreactive B cells, while cluster of differentiation [CD]-8+ T plays a role in platelet destruction through apoptosis. The classical pathway of the complement system also causes platelet destruction. By inhibiting platelet production, low levels of thrombopoietin and an immune response against megakaryocytes in the bone marrow worsen thrombocytopenia.

T-cell subset changes and an increase in activated autoreactive B cells, in addition to the function of components of the innate immune system [the complement system, dendritic cells, and natural killer cells], play a critical role in the pathogenesis of the ITP. Accurate detection of these changes may lead to developing new therapeutic strategies and identifying better prognostic/diagnostic factors.