Upregulation of FOXP3 is associated with severity of hypoxia and poor outcomes in COVID-19 patients
The levels of messenger RNA (mRNA) transcription of FOXP3, IFN-γ, TNF, IL-6 and COX-2 from both COVID-19 infected and control subjects were evaluated using SYBRTM green real-time polymerase chain reaction (RT-PCR). Severe/critical cases showed significantly lower lymphocyte counts and higher neutrop...
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Published in | Virology (New York, N.Y.) Vol. 563; pp. 74 - 81 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.11.2021
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Subjects | |
Online Access | Get full text |
ISSN | 0042-6822 1096-0341 1096-0341 |
DOI | 10.1016/j.virol.2021.08.012 |
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Summary: | The levels of messenger RNA (mRNA) transcription of FOXP3, IFN-γ, TNF, IL-6 and COX-2 from both COVID-19 infected and control subjects were evaluated using SYBRTM green real-time polymerase chain reaction (RT-PCR). Severe/critical cases showed significantly lower lymphocyte counts and higher neutrophil counts than the mild or moderate cases. There were significantly lower levels of mRNA expressions of IFN-γ, TNFα and FOXP3 in COVID-19 patients than in the control group. On the other hand, IL-6 and COX-2 expressions were significantly higher in patients suffering from severe disease. FOXP3 expressions were correlated with the severities of hypoxia and were excellent in predicting the disease severity. This was followed by the IL-6, COX-2 and TNFα expressions. FOXP3 expression was the only biomarker to show a significant correlation with patient mortality. It was concluded that SARS-CoV-2 infection is associated with the downregulation of FOXP3 and upregulations of IL-6 and COX-2.
•The immunological response to SARS-CoV-2 infection is still obscure.•Low mRNA expressions of IFN-γ, TNFα and FOXP3 were detected in COVID-19 patients.•IL-6 and COX-2 are highly expressed in patients suffering from severe COVID-19.•FOXP3 can be used as a potential biomarker for predicting disease severity.•COVID-19 coincides with downregulation of FOXP3 and upregulations of IL-6 and COX-2. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0042-6822 1096-0341 1096-0341 |
DOI: | 10.1016/j.virol.2021.08.012 |