Regular ArticleImbalance between CD205 and CD80/CD86 in dendritic cells in patients with immune thrombocytopenia

- Expression of CD205 was significantly decreased in monocytes-drived DCs in ITP.
- Expression of CD205 was significantly reduced or absent in ITP spleens.
- Loss of balance between CD205 and CD80/CD86 contribute to the pathogenesis of ITP.
- HD-DXM could rectify the loss of balance between CD205 and CD80/CD86 in ITP.

IntroductionCD205(DEC-205), a tolerance-associated receptor, is a member of the macrophage mannose receptor family of C-type lectin receptors. Antigen uptake via CD205 induces regulatory T cells, thereby regulating peripheral immune tolerance. However, the contribution of CD205 to autoimmune diseases has not been elucidated. Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by overdestruction of platelets. A previous study by the present authors found that CD205 expression in dendritic cells (DCs) was upregulated during induction of immune tolerance in patients with ITP.MethodsCD205 expression in monocyte-derived DCs and spleens from patients with ITP was analysed prior to and after high-dose dexamethasone (HD-DXM) treatment. Expression of CD80, CD86 and HLA-DR was also analysed in order to identify and define the maturation status of the DCs more precisely.ResultsIn patients with ITP, CD205 expression was found to be significantly decreased in DCs, and rare or absent in the border region of the spleen. However, the expression of CD80 and CD86 was increased in both monocyte-derived DCs and spleens in patients with ITP compared with controls. HD-DXM treatment may upregulate CD205 expression and downregulate CD80/CD86 expression, then rebalance the expression of CD205 and CD80/CD86 in DCs in patients with ITP.ConclusionImbalance between CD205 and CD80/CD86 may contribute to the development of ITP. Therapies that aim to restore the balance between CD205 and CD80/CD86 may help to re-establish tolerance in patients with ITP.