IL37,Tlymphocytes ,NK Cells in Pathogenesis of Immune Thrombocytopenia.

Idiopathic thrombocytopenia or immune thrombocytopenia (ITP) is a hematological condition which is characterized by a low platelet count of less than 100 x 109L . Symptoms of ITP can vary but tend to be symptoms of thrombocytopenia in general, such as petechiae, purpura, mucosal bleeding and in the most severe cases fatal intracranial hemorrhage(1,2) Interleukin (IL)-37, a novel anti-inflammatory cytokine previously known as interleukin-1 family member 7 before it was renamed, has a pivotal role in the suppression of immune responses (3,4). IL-37 is widely expressed in several types of cells, tissues and organs, including peripheral blood mononuclear cells (PBMCs) (5). The major role of IL-37 is to decrease excessive inflammation in innate and adaptive immune diseases, mainly by inhibiting the expression, production and function of pro-inflammatory cytokines, including IL-1α, IL-6, tumor necrosis factor (TNF) and macrophage inflammatory protein-2. The abundance of these cytokines has been reported to increase with the silencing of endogenous IL-37 in human blood cells (3,6).Aberrant expression of IL-37 has been observed in several inflammatory and autoimmune diseases However, the role of IL-37 in ITP has remained elusive. Immune thrombocytopenia pathogenesis is a complicated process. T cell immune abnormalities are involved in ITP pathogenesis. These abnormalities include platelet auto-antigen reactive cytotoxic T cells, abnormal numbers and functions of T regulatory cells, loss of Th1/Th2 balance, megakaryocyte maturation abnormalities and abnormal T cell anergy.