Primer immunologic defect in patients with idiopathic thrombocytopaenic purpura (ITP) result from autoreactive B-lymphocytes secreting antiplatelet antibodies. Dysfunctional cellular immunity has also great importance in ITP pathogenesis. CD4(+)CD25(+) regulatory T-cells have immunoregulatory features and it is able to inhibit CD4(+)CD25(-) and CD8(+) responses. ITP is also an autoimmune disease; the CD4(+)CD25(+) T-cell levels of the patients decrease during the active state. According to our findings, immunosuppressive treatments increase the CD4(+)CD25(+) Treg cell levels in the non-remission ITP patients. However, this level is not enough to overcome the resistance. CD4(+)CD25(-)Foxp3(+) and CD4(+)Foxp3(+) Treg cells are responsible for the pathogenesis of the non-remission ITP patients and other factors exist, which are responsible for the resistance of ITP treatment.