Prognostic Value of CD Markers in Immune Thrombocytopenic Purpura

Immune thrombocytopenia (ITP), previously called idiopathic thrombocytopenia purpura, is an autoimmune disorder characterized by a severe reduction in peripheral blood platelet count. In healthy individuals, normal platelet count ranges from 150-450 × 109/L, while in thrombocytopenia counts fall to less than 100 × 109/L ( Provan et al., 2010).

Based on duration, ITP is differentiated into three phases. Newly diagnosed ITP occurs within 3 months of diagnosis, persistent ITP is present 3-12 months after diagnosis, and chronic ITP lasts >12 months since diagnosis (Roberto, 2011).

Autoantibodies against platelet glycoproteins (GPs), including GPIIb/IIIa and GPIb/IX, have been considered to play a crucial role in ITP (Nomura, 2016) . In addition to platelet destruction, impaired maturation of megakaryocytes can be associated with reduced platelet production in ITP (Muna et al., 2015).

Furthermore, considerable attention has been recently paid to the dysregulation of a new B-cell subset known as regulatory B cells (Breg) in ITP (Li et al., 2012). This B-cell subset is characterized by CD19+CD38+ expression, promoting peripheral tolerance and reducing the function of autoreactive T-helper (Th) CD4+ cells via production of interleukin 10 (IL-10) (Flores-Borja et al., 2013). So they are an interesting cell population in diseases characterized by an unbalance in the immune system, such as autoimmune diseases, chronic infections, cancer and graft rejection.( Horikawa et al., 2013).

In ITP, as a result of the defective function of Breg and also Treg (regulatory T) cells, platelet autoreactive Th CD4+ cells undergo clonal expansion (McKenzie et al., 2013). so the presence of activated platelet-specific autoreactive T cells that respond to autologous platelet antigens participating in autoantibody production in ITP via interaction with autoreactive B cells (Solanilla et al., 2005).