Several studies have demonstrated T cell alteration and some features of immunosenescence in thalassemia major. Repeated alloimmunization converts naïve T-cells to memory cells and iron overload causes oxidative stress accelerating immune aging. To determine whether the alteration of T-cell cytokine is matched with early immune aging, the quantity of cytokine expressing T cells and their correlation to some immune aging markers were investigated. The proportion of IL2-and IFNc expressing CD4? and CD8? T-cells was measured in 27 hepatitis B, C and HIV negative B-thalassemia patients and a control group aged 10-30 years, following stimulation for 6 h with streptococcus enterotoxin B and intracellular cytokine staining. This proportion then were analyzed versus the percentage of the T-cells expressing each phenotyping marker, CD27, CD28, CD57 and CCR7. CD4? and CD8? positive T cells expressing IL-2 were significantly lower in b-thalassemia major compared to matched controls, but not T cells expressing IFNc. No significant difference was observed between splenectomized and non-splenectomized patients in cytokine expressing T cells. A negative correlation was noted between the percentage of T cells expressing IFNc and T-cells expressing CD-27, but not other markers. Lower T cells expressing IL-2 may reveal the decline of naïve and central memory T cells and is likely to be a feature of early immune aging. Decreased antigenic stimulation and iron overload may help to prevent this phenomenon.
Background: The fibrinogen receptor is an integrin on the platelet surface and is shaped from two types of glycoprotein (GP) subunits, GPIIb and GPIIIa. Membrane glycoprotein IIb/IIIa plays an important role in platelet function. The gene encoding the glycoprotein IIIa shows a common polymorphism, PLA2 that increases the binding of the receptor to fibrinogen and enhances the platelet aggregation. The clinical impact of PLA2 polymorphism has been studied in some diseases, but the definition of its exact role on venous thromboembolism complications has been challenging. The present systematic review aimed to clarify the association of PLA2 polymorphism and venous thromboembolism. Main text: In this study, Electronic databases including PubMed, Embase, Scopus, Web of Science, and Cochrane Library were searched. All the assessed studies focused on the relationship between PLA2 polymorphism and venous thromboembolism. Five studies were eligible for systematic review. One study revealed a significant correlation between PLA2 polymorphism and venous thromboembolism. PLA2 polymorphism was associated with deep vein thrombosis in one study and pulmonary thromboembolism in another one. Conclusion: The published data supported the hypothesis that having the PLA2 polymorphism of GPIIIa may be a risk factor for venous thromboembolism, but the association cannot be concluded; it needs more clinical investigation.
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