THE INTERLEUKIN-17F (7488T/C) GENE POLYMORPHISM AND THE RISK OF CHRONIC IMMUNE THROMBOCYTOPENIC PURPURA IN EGYPTIAN PATIENTS
                                                    
                        
            
            
                                    (Abstract release date: 05/19/16) 
                
                                    EHA Library. Yousry S.                     06/09/16;                    132978; E1429                
                
                
                
                
            
         
        
    
                     Prof. Sherif Yousry
Contributions
Contributions
                Abstract
            
         
        
    
                            Abstract: E1429
Type: Eposter Presentation
Background
Chronic primary immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by both reduced platelet counts and suppression of megakaryocyte and platelet development .IL-17F is a novel inflammatory cytokine and plays an important role in some autoimmune diseases by inducing the expression of multiple chemokines, cytokines, and adhesion molecules. IL-17F (7488T/C) polymorphism influence IL-17 expression and activity. Thus, considering the abnormal percentage of T helper 17 cells and the reported high levels of circulating IL-17F in patients with primary immune thrombocytopenia suggests a possible role of IL-17F (7488T/C) polymorphism in development of chronic ITP.
Aims
We investigated the role of IL17F polymorphism (7488T ⁄ C) on the susceptibility and clinical features of chronic ITP in Egyptian patients and if it may be linked to response to treatment with glucocorticoides.
Methods
A cohort of 107 patients with chronic ITP and 100 healthy control were enrolled in this case control study.Genotyping of IL17F (7488T/C) gene polymorphism was determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique
Results
Chronic ITP patients had a significantly higher frequency of the IL-17F 7488-TT genotype compared to controls (84.1% Vs 70.0%; Odd ratio= 2.269; P-Value = 0.015).Furthermore the IL17F 7488 TT genotype was significantly associated with poor response to corticosteroid therapy; 11.1% were steroid responsive vs. 88.9% were not responsive (P value= 0.001)
Conclusion
These findings suggest that the IL-17F 7488 T allele is significantly associated with the development of chronic ITP, suggesting a role for IL-17F polymorphism in the pathogenesis of chronic ITP.
Session topic: E-poster
Keyword(s): ITP, Polymorphism
                        Type: Eposter Presentation
Background
Chronic primary immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by both reduced platelet counts and suppression of megakaryocyte and platelet development .IL-17F is a novel inflammatory cytokine and plays an important role in some autoimmune diseases by inducing the expression of multiple chemokines, cytokines, and adhesion molecules. IL-17F (7488T/C) polymorphism influence IL-17 expression and activity. Thus, considering the abnormal percentage of T helper 17 cells and the reported high levels of circulating IL-17F in patients with primary immune thrombocytopenia suggests a possible role of IL-17F (7488T/C) polymorphism in development of chronic ITP.
Aims
We investigated the role of IL17F polymorphism (7488T ⁄ C) on the susceptibility and clinical features of chronic ITP in Egyptian patients and if it may be linked to response to treatment with glucocorticoides.
Methods
A cohort of 107 patients with chronic ITP and 100 healthy control were enrolled in this case control study.Genotyping of IL17F (7488T/C) gene polymorphism was determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique
Results
Chronic ITP patients had a significantly higher frequency of the IL-17F 7488-TT genotype compared to controls (84.1% Vs 70.0%; Odd ratio= 2.269; P-Value = 0.015).Furthermore the IL17F 7488 TT genotype was significantly associated with poor response to corticosteroid therapy; 11.1% were steroid responsive vs. 88.9% were not responsive (P value= 0.001)
Conclusion
These findings suggest that the IL-17F 7488 T allele is significantly associated with the development of chronic ITP, suggesting a role for IL-17F polymorphism in the pathogenesis of chronic ITP.
Session topic: E-poster
Keyword(s): ITP, Polymorphism
                        Abstract: E1429
Type: Eposter Presentation
Background
Chronic primary immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by both reduced platelet counts and suppression of megakaryocyte and platelet development .IL-17F is a novel inflammatory cytokine and plays an important role in some autoimmune diseases by inducing the expression of multiple chemokines, cytokines, and adhesion molecules. IL-17F (7488T/C) polymorphism influence IL-17 expression and activity. Thus, considering the abnormal percentage of T helper 17 cells and the reported high levels of circulating IL-17F in patients with primary immune thrombocytopenia suggests a possible role of IL-17F (7488T/C) polymorphism in development of chronic ITP.
Aims
We investigated the role of IL17F polymorphism (7488T ⁄ C) on the susceptibility and clinical features of chronic ITP in Egyptian patients and if it may be linked to response to treatment with glucocorticoides.
Methods
A cohort of 107 patients with chronic ITP and 100 healthy control were enrolled in this case control study.Genotyping of IL17F (7488T/C) gene polymorphism was determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique
Results
Chronic ITP patients had a significantly higher frequency of the IL-17F 7488-TT genotype compared to controls (84.1% Vs 70.0%; Odd ratio= 2.269; P-Value = 0.015).Furthermore the IL17F 7488 TT genotype was significantly associated with poor response to corticosteroid therapy; 11.1% were steroid responsive vs. 88.9% were not responsive (P value= 0.001)
Conclusion
These findings suggest that the IL-17F 7488 T allele is significantly associated with the development of chronic ITP, suggesting a role for IL-17F polymorphism in the pathogenesis of chronic ITP.
Session topic: E-poster
Keyword(s): ITP, Polymorphism
      
                
                    
                
                    
                
                
            Type: Eposter Presentation
Background
Chronic primary immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by both reduced platelet counts and suppression of megakaryocyte and platelet development .IL-17F is a novel inflammatory cytokine and plays an important role in some autoimmune diseases by inducing the expression of multiple chemokines, cytokines, and adhesion molecules. IL-17F (7488T/C) polymorphism influence IL-17 expression and activity. Thus, considering the abnormal percentage of T helper 17 cells and the reported high levels of circulating IL-17F in patients with primary immune thrombocytopenia suggests a possible role of IL-17F (7488T/C) polymorphism in development of chronic ITP.
Aims
We investigated the role of IL17F polymorphism (7488T ⁄ C) on the susceptibility and clinical features of chronic ITP in Egyptian patients and if it may be linked to response to treatment with glucocorticoides.
Methods
A cohort of 107 patients with chronic ITP and 100 healthy control were enrolled in this case control study.Genotyping of IL17F (7488T/C) gene polymorphism was determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique
Results
Chronic ITP patients had a significantly higher frequency of the IL-17F 7488-TT genotype compared to controls (84.1% Vs 70.0%; Odd ratio= 2.269; P-Value = 0.015).Furthermore the IL17F 7488 TT genotype was significantly associated with poor response to corticosteroid therapy; 11.1% were steroid responsive vs. 88.9% were not responsive (P value= 0.001)
Conclusion
These findings suggest that the IL-17F 7488 T allele is significantly associated with the development of chronic ITP, suggesting a role for IL-17F polymorphism in the pathogenesis of chronic ITP.
Session topic: E-poster
Keyword(s): ITP, Polymorphism
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