Background: IL-17 is an inflammatory cytokine that plays a crucial role in many autoimmune diseases. Aim: To investigate the association of IL-17A rs2275913 and IL-17F rs763780 gene polymorphisms with acute immune thrombocytopenic purpura (ITP) in Egyptian children. Patients and methods: We examined 80 patients (male/female, 33/47; median age, 7 years old) diagnosed with acute ITP and 55 healthy controls (male/female, 28/27; median age, 7 years old). Genotyping was determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: In the acute ITP group compared to control, statistical analysis of the genotype frequencies (GG, AG, AA) of the IL-17A rs2275913 polymorphism and its alleles (A, G) showed no significant difference between the two groups (p > 0.05). Interestingly, the IL17A rs2275913 GG genotype was associated with early recovery (p = 0.04). As regard the genotype frequencies of the IL-17F rs763780 polymorphism, there was statistical significant difference in the TT and TC genotype frequencies between the case and control groups (p = 0.001 and p = 0.003, respectively). The number of IL-17F rs763780 T alleles was significantly higher in acute ITP patients as compared with children in the control group (p < 0.001). Conclusion: The present findings indicate that the IL-17 polymorphism IL-17F rs763780, but not IL-17A rs2275913 may be associated with a higher risk of acute ITP in Egyptian children.
Background and objectivesIL27 and IL35 are regulatory T cells (T-regs) related cytokines; they were accused in eukemogenesis of acute myeloid leukemia (AML). This study aimed to assess the expression of these cytokines in de novo AML and investigate their role as biomarkers.Subjects and methodsSeventy newly diagnosed patients with primary AML and 30 matched healthy volunteers were recruited. AML diagnosis was confirmed with flowcytometric and immunophenotypic analyses, while ELISA was used to assess serum levels of IL27 and IL35 in patients and controls. Receiver operating characteristic curve analysis was used to estimate IL27 and IL35 optimum cutoff values for predicting AML.ResultsSerum levels of both cytokines were significantly higher in AML patients than controls (P<0.001), with no effect of gender or French-American-British subtypes. Significant correlations of IL27 and IL35 with poor prognostic factors and with each other were detected in patients only. IL27 optimum cutoff for predicting AML was >43, AUC (0.926) with a sensitivity 74% and specificity 96.6% (P<0.001), while for IL35>27.8, AUC (0.972) with 88% and 98% sensitivity and specificity, respectively (P<0.001).ConclusionConclusively, this study proved that IL27and IL35 could identify AML patients from healthy subjects, and their overexpression denotes poor prognosis. Based on the simplicity and wide availability of their detection technique we recommend the inclusion of IL27 and IL35 in the diagnostic/prognostic workup of AML; however, further longitudinal research is needed to prove their exact prognostic value.
Primary immune thrombocytopenia (ITP) is a common condition characterized by a low peripheral platelet count (100000/L) caused by cell-mediated and humoral-mediated destruction of the platelet. Immunological tolerance to platelet antigens is lost in these patients. The main step in the pathogenesis includes the overactivation of T-cells, particularly T-helper cells, the release of various cytokines, and the interaction of autoantibodies with platelet surface antigens, which results in platelet destruction by the immune system in the spleen. The most common PLT antigens against which autoantibodies are directed are CD41 and CD61. These antigens are occupied by autoantibodies so there is decreased detection of these antigens on the surface of platelets. PD1 is an important negative stimulatory molecule of the immune system a member of the CD28/B7 family. ITP patients have considerably increased levels of PD-1 on CD4+Tcells in their peripheral blood than healthy people., indicating that the PD1 molecule plays an important role in illness etiology.
Background The sickle cell trait (SCT) disorder possesses a clinical heterogeneity ranging from a symptomless condition to sudden death. This study aimed to develop a diagnostic approach that helps the characterization and identification of SCT from normal subjects and sickle cell disease (SCD) patients, and to assess its severity. Methods Sixty controls, 24 SCD patients and 31 SCT subjects were assessed clinically, radiologically and by laboratory investigations. Results Of the SCT subjects, 12.8% were symptomatic (3.2% anemic, 6.4% hemolytic crisis, and 3.2% painful crises). Anemia was normocytic in 66.6%, and normochromic and polychromatic in 33.4%. Significantly lower red blood cells (RBCs), hemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), hematocrit (Hct), Shine and Lal index (SL), and hemoglobin A (Hb A), and higher mean corpuscular hemoglobin concentration (MCHC), red cell distribution width (RDW), Ricerca index (RI), and Huber-Herklotz index (HH) were found in SCT subjects compared with the controls. Hb A and hemoglobin S (Hb S) were excellent in discriminating SCT from SCD (cut-off for SCT > 50% and < 40%) followed by Hct, MCHC, Hb, Green and King index (GK), and England and Fraser index (EF) (cut-off for SCT > 33%, > 32, > 11, < 71, and < 10, respectively). Radiologically normal findings were detected in 87% of SCT subjects; they had nearly normal liver and renal function tests (except one case each). A schematic diagnostic paradigm for SCT was proposed. Conclusion This study allowed understanding of SCT in various aspects, i.e., clinical, hematological, biochemical and radiological. Thus, it could help prevention of the Hb S variant disorder and proper management of carriers. This might be applied in pre-marital screening, particularly in those with family history of Hb S disorder.
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