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Table 1 Role of immune soluble mediators in COVID-19 infection

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

[15,16,17,18, 21]

sPD-1

Increase effector T lymphocytes function

Adverse effect

[15, 19, 20]

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

[19, 24,25,26]

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

[28, 30,31,32,33,34]

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

[36,37,38,39,40]

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

[43,44,45,46,47,48]

  1. sPDL-1, soluble programmed cell death ligand 1; sPD-1, soluble programmed cell death 1; sTim3, soluble T-cell immunoglobulin and mucin domain 3; sTNFRI&II, soluble tumor necrosis factor receptor 1&2; sIL6R, soluble interleukin 6 receptor