الفهرس 
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Abstract
Systemic lupus erythematosus (SLE) is a prototypic multisystemic autoimmune disease that can affect many cells, tissues and organs by the production of multiple autoantibodies against various cellular components such as nucleic acids and nuclear proteins. A complex interaction of genetics, environment, and hormones leads to immune dysregulation and breakdown of tolerance to self-antigens, resulting in autoantibody production due to imbalance between apoptotic cell production and clearance of apoptotic material. IL-10 has a dual function, it has a positive influence on B cell survival, proliferation, differentiation, and autoantibody production, also it downregulates the T lymphocyte cells response. It is noticed that the concentration of plasma IL-10 in SLE is elevated and correlated with disease activity (SLEDAI) and anti-dsDNA antibodies production. Platelets are capable of modulating adaptive and innate immune responses via various mechanisms with evidences suggest that platelets are activated in SLE and contribute to SLE pathogenesis. It has been proved that release of CD40L is hallmarks of platelet activation which is associated with disease severity and the development of nephritic lupus in SLE patients. Platelets through sCD40L can directly modulate humoral activity, stimulating B cell proliferation, antibody production, Furthermore, through CD40-CD40L ligation, platelets support B cell isotype switching and enhance germinal center formation, with the collaboration of Th cells. Platelets can bind to lymphocytes via P-selectin/PSGL-1 interaction. However, other molecules, such as CD40-CD40L, GPIb-CD11b, and GPIIb/IIIa-CD11/CD18, can also play a role in the binding of platelet to lymphocytes. An elevated number of circulating lymphocyte-platelet complexes and an increased platelet activation have been reported in patients with SLE and other autoimmune diseases. However, the binding of platelets to different lymphocyte subpopulations in SLE patients has not yet been studied and there is a lack of information about the relationship between platelet-binding to lymphocytes, lymphocyte function, and the clinical outcome of these patients. So, the aim of this study is to analyze the possible role of plateletlymphocyte binding and platelet activation in pathogenesis of SLE, clarifying their relationship to the clinical and laboratory features of SLE patients. This study was carried at clinical pathology department in Tanta University. It included 30 patients with systemic lupus erythematosus who attended to internal medicine department and Physical Medicine, Rheumatology & Rehabilitation Department in Tanta University Hospital and 30 healthy control individuals. All patients will be subjected to the following: 1. Full history with special emphasis on age, sex, symptoms of SLE and disease duration. 2. Clinical examination: All patients were examined to evaluate SLE and exclude other diagnosis. 3. Disease activity was assessed by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) at the time of the sample collection. 4. Routine laboratory investigations; CBC, ESR, CRP, C3, C4, antidsDNA, ANA and albumin/creatinine ratio. 5. Specific laboratory tests include flow cytometric analysis of the peripheral blood samples to detect lymphocytes bound to platelets and measurement of serum concentrations of IL-10 and sCD40L by specific ELISA kits. In this thesis, comparative studies were done between the SLE patient group and control healthy group as regard percentages of circulating B and T lymphocytes with bound platelets, sCD40L, IL10, CBC, inflammatory markers, urea and creatinine. Correlations of the percentages of circulating B and T lymphocytes with bound platelets, sCD40L and IL10 with each other and with other parameters were done. Also, this study analyzed the relationship between lymphocytes with bound platelets and disease activity as SLDAI, presence of hematuria and laboratory features as complement 3, complement 4, anti-double strand DNA (Anti-dsDNA) and albumin/creatinine ratio. The following results were obtained: There was no significant difference between SLE patients and control group regarding age and gender As regard inflammatory markers, ESR showed a significant increase in SLE patients compared to control group, while there was no significant difference in CRP between the two studied group. As regard CBC, Hemoglobin, platelet count and leucocytic count showed significant decrease in SLE patients compared to controls. Furthermore, the percentage of total, B and T lymphocytes decreased significantly in association with SLE. Alternatively, both creatinine and urea levels showed a significant increase in SLE patients compared to controls. There was a significant increase in the percentage of lymphocyte bound platelets (CD19+CD41a+ lymphocytes and CD3+CD41a+ lymphocytes), sCD40L level and IL10 level in SLE patients compared to controls. Also, the percentage of lymphocyte bound platelets, sCD40L and IL10 expressed a significant increase in SLE patients who had hematuria and positive anti-dsDNA compared to SLE patients without hematuria and negative anti-dsDNA. Both sCD40L and IL10 had a significant positive correlation with each other and with CD19+CD41a+ lymphocytes, CD3+CD41a+ lymphocytes, albumin to creatinine ratio, SLEDAI, creatinine and urea, while they had a significant negative correlation with C3, C4, hemoglobin, platelets and leucocytic count. CD19+CD41a+ lymphocytes and CD3+CD41a+ lymphocytes had a significant positive correlation with each other and with sCD40L, IL10, albumin to creatinine ratio, SLEDAI, creatinine and urea, while they had a significant negative correlation with C3, C4 and platelets. Moreover, CD3+CD41a+ lymphocytes had a significant negative correlation with leucocytic count.