الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Immune thrombocytopenia is a heterogeneous autoimmune disease, characterized by immune cell-mediated platelet destruction and/or platelet production defect, leading to a lower platelet count, putting patients on a higher risk of bleeding.
The pathological mechanisms underlying the development of immune thrombocytopenia (ITP) are unclear and its diagnosis remains a process of exclusion. Currently, there are no known specific biomarkers for ITP to support differential diagnosis and treatment decisions.
T lymphocyte abnormalities are considered an important factor in the pathogenesis of ITP. Only about 60% of patients with ITP have detectable plasma and/or platelet-bound autoantibodies, suggesting a non-antibody-mediated mechanism of ITP.
Th17 and associated IL-17 were involved in the pathogenesis of ITP. RUNX1, a member of the runt domain containing family of transcription factors, is required for Th17 differentiation via interacting with a master regulator of Th17, RORγt.
This study aimed to study the expression of RUNX1 and RORγt in patients with ITP and to determine their relevance to the pathogenesis of the disease.
This study was carried on 60 subjects from the Alexandria University children hospital divided into 2 groups: 30 subjects with newly diagnosed active ITP (group I) and 30 patients in remission after treated with corticosteroids or IVIG (group II). In addition 30 age and sex matched healthy controls were included.
CBC was done for patients and control then peripheral blood mononuclear cells (PBMCs) were isolated from both patients and controls to measure mRNA level of RUNX1 and RORγt by quantitative real-time PCR.
In our study we demonstrated a significantly higher expression of RUNX1and RORγt genes in newly diagnosed active ITP patients compared to ITP patients in remission and normal controls. Furthermore there is a significant positive correlation of RUNX1 with RORγt in active ITP patients indicating cooperative interaction between the two genes in the pathogenesis of the disease.
Our results indicated that RUNX1 might be involved in the pathogenesis of ITP through interaction with RORγt, the master regulator of Th17, and targeting them may be a new therapeutic approach in the treatment of ITP.