الفهرس 
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Abstract
Primary immune thrombocytopenia (ITP) is an autoimmune mediated bleeding disorder characterized by thrombocytopenia which is the result of increased platelet destruction and decreased platelet production by antiplatelet autoantibodies.
The pathophysiology of ITP is heterogeneous and complex. While the presence of antibodies against platelet glycoproteins has traditionally been considered to play a central role, several abnormalities in the cellular mechanisms of immune modulation have been described.
Among these abnormalities, are the increased number of the T helper 1(Th1) cells, the decreased number or defective suppressive function of regulatory T cells, and the platelet destruction by cytotoxic T lymphocytes (CTL). Also dysregulated T-cells in patients with ITP may enable the development of platelet autoantibodies, have a direct cytotoxic effect on platelets, and impair platelet production by megakaryocytes. CD4+ helper T cells are usually classified into two subsets based on the types of cytokines they produced. T helper 1 (Th1) cells produce interferon (IFN)-γ, IL2, GM-CSF, and TNF and are mainly involved in macrophage activation, while T helper 2 (Th2) cells produce IL4, IL5, IL6, IL10, and IL13 and mainly induce antibody production. The balance between Th1 and Th2 subsets has been implicated in the regulation of many immune responses (Mosmann and Sad, 1996), and is known to be impaired in various autoimmune diseases. The polarization of the immune system towards either cellular (Th1) or humoral (Th2) immunity is dependent on the level of the cytokines at the site of immune activation. Several reports on serum cytokines in ITP have pointed towards a specific Th-cell activation. Some studies suggested a less prominent Th1 response (Nomura et al., 1995) or even found a Th2 response in patients with chronic ITP (Webber et al., 2001), but most investigations described a higher Th1 response (Stasi et al., 2007).
Recently, a novel subset of CD4+ T cells, distinct from Th1 and Th2 cells, was identified, characterized by the production of interleukin 17 (IL-17) and, therefore, designated as Th17 cells. Th17 has been shown to play a crucial role in the induction of autoimmune diseases (Park et al., 2005) .
It is now proposed that there are populations of regulatory T cells (T-reg), some designated T-helper type 3 (Th3), that exert their action primarily by secreting TGF-beta1. TGF-beta1 has multiple suppressive actions on T cells, B cells, macrophages, and other cells, and increased TGF-beta1 production correlates with protection and/or recovery from autoimmune diseases ( Prud home and Piccirillo, 2000 ).
Transforming growth factor-β1 is reduced and interleukin-17 and interferon-γ is elevated in pediatric patients with active chronic primary immune thrombocytopenia ( Wang et al., 2011),while ITP in remission was associated with elevated TGF-beta1 suggesting a role for these cytokines in remission of chronic idiopathic thrombocytopenic purpura ( Andersson et al., 2000 ).
Interestingly, approximately 40% of patients with ITP have no identifiable auto antibodies, yet they have extremely low platelet counts.
In these patients, platelet destruction was mediated by CD8+ T cells suggesting, for the first time, an entirely new mode of platelet destruction (cell mediated cytolysis of platelets) ( Olsson et al., 2003).
This study was carried out on 90 subjects divided into two groups the first group consists of 45 patients with chronic and persistent ITP, the second group consists of 45 normal healthy controls.
All participants were subjected to careful history taking, thorough clinical examination and appropriate laboratory investigations including CBC and assessment of serum levels of IL-17 and TGF beta 1 using ELISA technique.
Our results revealed that as regards to interleukin 17 levels, there was a statistically significant difference between the cases and control groups where the cases levels were significantly higher.
As regards to interleukin TGF levels, also there was a statistically significant difference between the two studied groups where the cases levels were significantly higher.
This suggests that IL-17 and TGF may have a role in the pathogenesis of ITP through induction or promotion of the generation of pro-inflammatory T-cells.