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العنوان
Immunological Studies In Egyptian Patients With Autoimmune Rheumatic Disease \
المؤلف
Kassem, Sara Fathi Mohamed.
هيئة الاعداد
باحث / Sara Fathi Mohamed Kassem
مشرف / Ahmed Abbas Rauf
مشرف / Roba Mohamed Talaat
مناقش / Ahmed Mohamed Osman
مناقش / Elsayed Mohamed Elsayed Mahdy
الموضوع
Rheumatism. Rheumatic Diseases.
تاريخ النشر
2015.
عدد الصفحات
142 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
Molecular Biology
تاريخ الإجازة
1/5/2015
مكان الإجازة
جامعة مدينة السادات - معهد بحوث الهندسة الوراثية - Molecular Biology Department
الفهرس
Only 14 pages are availabe for public view

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Abstract

Imbalance of T-helper-cell (TH) subsets (TH1/TH2/TH17) and regulatory T-cells (Tregs) is suggested to contribute to the pathogenesis of Systemic lupus erythematosus (SLE). Therefore, cytokine secretion profile in SLE patients and their possible association with disease activity were evaluated. Sixty SLE patients, 24 rheumatoid arthritis (RA) patients and 24 healthy volunteers were included in this study. Demographic, clinical, disease activity and serological data were prospectively assessed. Plasma cytokines levels of TH1 (IL-12, IFN- γ), TH2 (IL-4, IL-6, IL-10), TH17 (IL-17, IL-23) and Treg (IL-10 and TGF-β) were measured by enzyme linked immunosorbent assays (ELISA). SLE patients were found to have significantly higher levels of IL-17 (p<0.001), IL-6 (p<0.01), IL- 12 (p<0.001) and IL-10 (p<0.05) but comparable levels of IL-23 and IL-4 and slight reduction (but statistically insignificant) of TGF- β levels compared to controls. IL-6, IL-10 and IL-17 were significantly increased (p<0.05) with disease activity. The RA group exhibited significantly higher levels of plasma IL-4 (p<0.01), IL-6 (p < 0.05), IL-17 (p<0.001), IL-23 (p<0.01) and TGF- β (p<0.5) and lower IFN- γ (p<0.001) and IL-10 (p<0.01) than those of healthy subjects. This study showed a distinct profile of cytokine imbalance in SLE patients. Reduction in IFN-γ (TH1) and TGF- β (Treg) with the elevation in IL-6 and IL-17 (TH17) could imply skewing of T-cells toward TH17 cells. Breaking TH17/Treg balance in peripheral blood may play an important role in the development of SLE and could be responsible for an increased pro-inflammatory response especially in the active form of the disease.