IL-6: This pro-inflammatory cytokine has been found to be elevated in severe COVID-19 patients and in chronic COVID patients. [Patterson, et al., IJID 2020; Patterson, et al., Front. Immunol. 2021].

IFN-gamma: This pro-inflammatory cytokine has been found to be elevated in chronic COVID patients. [Patterson, et al., IJID 2020 Patterson, et al., Front. Immunol. 2021]

IL-2: This is responsible for proliferation and activation of T cells, B cells and NK cells.

IL-4: The interleukin 4 is a cytokine that induces differentiation of naive helper T cells to Th2 cells. Upon activation by IL-4, Th2 cells subsequently produce additional IL-4 in a positive feedback loop. IL-4 is produced primarily by mast cells, Th2 cells, eosinophils, and basophils.

CXCL8 (IL-8): Interleukin 8 is a chemokine produced by macrophages and other cell types such as epithelial cells, airway smooth muscle cells and endothelial cells. Endothelial cells store IL-8 in their storage vesicles, the Weibel-Palade bodies. In humans, the interleukin-8 protein is encoded bythe CXCL8 gene.

IL-10: This has been found to be elevated in chronic COVID patients. [Patterson, et al., Front. Immunol. 2021]. It has been observed that long-hauler patients demonstrate an elevation in IL-2 and IFN-gamma and a reduction in CCL4.

IL-13: This is a cytokine produced by Th2 cells, NK cells, mast cells, basophils and is a mediator of allergic inflammation and a key regulator of IgEsynthesis, mucus hypersecretion, and airway hyperresponsiveness. [Rael et al., Gulati, et al.,]

GM-CSF: This is is produced by T cells, macrophages and fibroblasts and stimulates production of granulocytes, monocytes, and eosinophils [Turner, etal.,]. GM-CSF has been found to be reduced in chronic COVID patients. [Patterson, et al., Front. Immunol. 2021].

CCL3: This is involved in macrophage and NK-cell migration as well as T-cell dendritic cell interactions [Sokol, et al.,]. It also has been found to be elevated in chronic COVID patients. [Patterson, et al., Front. Immunol. 2021].

CCL4: This has been found to be reduced in chronic COVID patients. [Patterson, et al., Front. Immunol. 2021] CCL4 is involved in macrophage andNK-cell migration as well as T-cell/dendritic cell interactions [Sokol, et al.,]. CCL4 signals through the receptor CCR5 to attract T cells to the site of inflammation and depending on the immune context, can recruit differentially activated T cells [Patterson, et al., Front. Immunol.; Liu, et al; Mukaida,et al.,]

CCL5: This is involved in macrophage and NK-cell migration as well as T-cell/dendritic cell interactions [Sokol, et al.,] CCL5 levels have been found to be highly elevated in severe COVID-19 patients, but not in chronic COVID patients. [Patterson, et al., Front. Immunol. 2021; Patterson, et al., IJID2020)

VEGF: This has been found to be elevated in chronic COVID patients. [Patterson, et al., Front. Immunol. 2021]. The presence of VEGF in inflammation neuropathies such as ClOP, GBS and vascular neuropathy may indicate a potential relation with vascular involvement. [Nobile-Orazio, et al.,] VEGF has been shown to be elevated in POEMS but no other monoclonal gammopathies and can be elevated in immune- mediated neuropathies.

TNF-alpha: This is a pro-inflammatory cytokine, associated with phagocyte cell activation and endotoxic shock. [Turner, et al.,) TNF-alpha has been shown to play a role in the process of pathological pain. [Zhang, et al.,]

sCD40L: Soluble CD40 ligand (sCD40L) is contained in platelet granules and thus its presence in the blood is a marker of platelet activation. By interacting with CD40, which is found on endothelial and smooth muscle cells, sCD40L may trigger the release of inflammatory mediators, lead to increased activity of matrix metalloproteinases, and activate the coagulation