From: Immune system-related soluble mediators and COVID-19: basic mechanisms and clinical perspectives
Soluble mediator | Biological role in COVID-19 infection | Output effect | References |
---|---|---|---|
sPDL-1 | Decrease of effector T lymphocytes Increase in lower PaO2/FIO2 ratio and higher CRP concentration | Protective effect | |
sPD-1 | Increase effector T lymphocytes function | Adverse effect | |
sTim-3 | Activation and exhaustion marker of T lymphocytes in chronic inflammation and viral infection like SARS-CoV-2 Negative and positive correlation with PaO2/FIO2 ratio and NT-ProNBT, respectively | Adverse effect | |
sTNFRI and sTNFRII | Increase in COVID-19 cases Cleaved by ADAM17 in chronic inflammation Increased mortality risk in cardiovascular diseases Correlate with illness severity iv COVID-19 cases | Adverse effect | |
sIL-2R | Increase in COVID-19 cases Cause to lymphopenia and reduced cell response to IL-2 Negative regulator of regulatory T lymphocytes, NK cells, and B lymphocytes Negative association with PaO2/FiO2 ratio Positive correlation with morbidity in COVID-19 cases | Adverse effect | |
sIL-6R | Role in stromal epithelial response to IL-6 Agonist of IL-6 which is cleaved by ADAM17 Increase in HIV, influenza A, and severe COVID-19 cases Cause to increased release of MCP-1 from endothelial cells in COVID-19 cases ( cause to hyper inflammation) | Adverse effect |