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Background: COVID-19 causes a range of clinical symptoms from mild to critical and can be life-threatening. Up to now, it has led to many deaths. We aimed to evaluate exhausted markers on CD4 + T cells of COVID-19 patients.Methods: In this study, we evaluated 44 patients with confirmed COVID-19 disease and 16 healthy individuals. Patients were divided into moderate/severe and critical groups. Peripheral blood mononuclear cells (PBMCs) were isolated and stained by anti-human CD39, PD-1, TIM-3, and anti-human CD4. The percentage of each CD4 + subpopulation was calculated by flow cytometry. Furthermore, we collected clinical information and laboratory data of both control and patient groups.Results: We detected overexpression of TIM-3 on CD4 + T cells in both critical and moderate/severe patients than in healthy individuals (HIs; p < .01 and p < .0001, respectively). CD4 + TIM-3 + CD39 + lymphocytes were significantly higher in the critical patients than in HI (p < .05). Both Patient groups showed lymphopenia in comparison with HI, but CD4 + lymphocytes did not show any significant difference between study subjects. The increased amount of

Background During viral infection, inhibitory receptors play a key role in regulating CD8 T-cell activity. The objective of this research was to investigate programmed cell death protein 1 (PD-1), mucin domain-containing protein-3 (TIM-3), and CD39 exhaustion markers in CD8 T cells of new coronavirus disease-2019 (COVID-19) patients. Methods A total of 44 patients with COVID-19 (17 subjects in a critical group and 27 patients in a non-critical group) and 14 healthy controls, who were admitted to Hospitals in Babol, were recruited to the study. In subjects' peripheral blood mononuclear cells (PBMCs), we compared the phenotype of CD8 T lymphocytes, expressing PD-1, TIM-3, or CD39, both alone and in various combinations. Results The findings showed that the percentage of CD8 + cell counts was significantly lower in non-critical patients. Critical and non-critical patients were more likely than healthy controls to have an escalated frequency of CD8 + TIM-3 + , CD8 + CD39 + , and CD8 + TIM-3 + CD39 + cells. No significant differences were observed between all groups in the CD8 + PD-1 + cell counts. There was also no difference between three groups regarding the counts of CD8+TIM-3+PD-1 + , CD8 + PD-1 + CD39 + , and CD8 + TIM-3 + PD-1 + CD39 + cells. The counts of non-exhausted cells were significantly lower in critical and non-critical individuals compared to the healthy individuals’ value. Conclusion Patients, infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), altered exhausted CD8 T lymphocytes with CD39 and TIM-3 exhaustion markers, which may account the dysregulated immune response found in COVID-19.

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Pentraxin 3 (PTX3) and ficolin are the plasma phase of pattern recognition receptors (PRRs) and can activate complement through classical and lectin pathways, respectively, which may contribute to disease severity. This study aimed to investigate the association between PTX3 and ficolin with disease severity in patients with coronavirus disease-2019 (COVID-19). Seventythree COVID-19 patients and 25 healthy controls were enrolled in this study. The participants were divided into three groups as follows: 14 patients as the intensive care unit (ICU) group, 59 patients as the non-ICU group, and 25 subjects as the healthy control group. The serum levels of PTX3 and ficolin were measured by enzyme-linked immunosorbent assay (ELISA) kits. Patients in ICU and non-ICU groups had significantly higher levels of PTX3 compared to the healthy control group (p = 0.0002 and p = 0.0072, respectively). Patients in the ICU group also had an increased amount of PTX3 (1957 ± 1769 pg/ml) compared to non-ICU patients (1220 ± 1784 pg/ml). However, this difference was not significant. On the other hand, serum levels of ficolin were not different among the three groups. PTX3, as an acute phase protein, may contribute to disease severity. Its probable inflammatory role could result from the high activation of the complement system. On the other hand, it could be suggested that ficolin has no crucial role in the disease severity of COVID-19 patients.