The role of autophagy-related markers Beclin-1, LC3, and P62 in the pathogenesis of immune thrombocytopenia in children.

BACKGROUND

Immune thrombocytopenic purpura (ITP) is an autoimmune disorder in which thrombocytopenia results from antiplatelet autoantibody-mediated destruction and/or suppression of platelet production. Autophagy also plays an important role in the regulation of the innate and adaptive immune systems, and when autophagy becomes inefficient, it may lead to diverse autoimmune diseases.

OBJECTIVES

We aimed to assess autophagy-related markers Beclin-1, LC3, and P62 expression in ITP and to investigate the relation between autophagy markers and antiplatelet autoantibodies in pediatric ITP.

METHODS

Gene expressions of Beclin-1, LC3, and P62 messenger RNA were assessed by quantitative real-time polymerase chain reaction in 30 children diagnosed with ITP and 20 healthy controls.

RESULTS

The results showed that the relative gene expression of both Beclin-1 and LC3 genes was significantly increased in ITP patients compared with the control group, while P62 relative gene expression was significantly decreased in ITP patients compared with the control group. The relative gene expression of Beclin-1 and LC3 was significantly increased in ITP patients with positive antiplatelet antibodies compared with those with negative antiplatelet antibodies, while the relative gene expression of P62 was significantly decreased in ITP patients with positive antiplatelet antibodies compared with those with negative antiplatelet antibodies.

CONCLUSION

The results demonstrated a possible role of dysregulation of autophagy genes in the pathogenesis of ITP. Furthermore, the correlation between impaired autophagy and autoantibodies, a known mechanism of the pathogenesis of ITP, supports a possible role of impaired autophagy in the pathogenesis of ITP.