ABSTRACT
Severity of symptoms in COVID-19 has been shown to result from a cytokine storm. Interleukin (IL)-17 is one of these various cytokines, which results in a proinflammatory response, systemic inflammatory symptoms, inflammatory cell infiltration of lung tissue and thus leads to the massive lung pathology and multiorgan failure. Gene polymorphisms in the regulatory regions of cytokine-encoding genes affect the amounts of cytokines produced and possess a fundamental role in infectious diseases. This study aimed to investigate the role of IL-17A (rs2275913;G197A) gene polymorphism as predictor of disease severity and its correlation with IL-17 serum levels in COVID-19 patients. A group of 70 COVID-19 patients and 17 age and sex-matched control subjects were enrolled in the present work. Patients were classified into two groups moderate, severe and acute respiratory distress (ARDS) cases, defined according to the criteria established by the world health organization. Quantitative real time-polymerase chain reaction was done to detect IL-17A (rs2275913;G197A). Serum IL-17 levels were assessed by an enzyme-linked immunosorbent assay in both patients and controls. The distribution of different IL-17A G/A genotypes among COVID-19 patients were 44.3% for GG genotype, 44.3% for AG genotype and 11.4% for AA genotype. Genotypes among the control group were 43.8% for GG genotype, 50% for AG genotype and 6.3% for AA genotype. G allele distribution was 66.4%, 68.8% in patient and control group, respectively, and A allele was 33.6% and 31.3%, respectively. There was no association between the different genotypes, disease severity or IL-17 serum levels in the patient group. In conclusion, despite the possible role of IL-17 in the pathogenesis of inflammation, there was no association between IL-17 polymorphism and disease severity or IL-17 serum levels among Egyptian COVID-19 patients.
ABSTRACT
NK group 2 member A (NKG2A) receptor transduces inhibitory signaling;suppressing NK and T-cell cytokine secretion and cytotoxic function. This study aimed to assess the expression of NKG2A inhibitory receptor on natural killer (NK) cells and CD8+ T lymphocytes in COVID-19 patients and correlate the results with disease severity defined according to the criteria established by the world health organization, in a trial to understand the immunological response towards COVID-19 infection. The study enrolled 30 COVID-19 patients classified into 2 groups that comprised 15 subjects each;moderate and severe based on clinical, radiological, and laboratory findings. Ten age and sex matched apparently healthy individuals were included in this study as a control group. About 1 ml EDTA anti-coagulated blood samples were collected for measuring expression of NKG2A/CD159a on CD56+ CD3- NK and CD3+CD8+ T cells by flow cytometry. Results revealed that COVID-19 patients had significantly lower NK and CD8+ T cell counts compared to healthy subjects. Severe cases had significantly lower CD8+ T counts compared to moderate ones. Percentages of NK and CD8+T cells expressing NKG2A receptor were significantly higher in cases compared to controls. Comparison between severe and moderate cases revealed that although the percentages of NK cells expressing NKG2A receptor were not significantly higher in severe cases, the mean fluorescence intensity was significantly higher. The percentages of CD8 +T cells expressing NKG2A receptor were significantly higher in severe cases with higher mean fluorescence intensity. In conclusion, our results indicate that elevated NKG2A expression on cytotoxic lymphocytes correlates with disease severity in COVID-19 patients, and may serve as a potential marker for prognosis. Additionally, the blockade of NKG2A should be investigated as means of enhancing NK cell and cytotoxic T cells antiviral immunity in patients with severe COVID-19 infection. Copyright© by the Egyptian Association of Immunologists.