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Fig. 2 | Clinical Epigenetics

Fig. 2

From: Management of epigenomic networks entailed in coronavirus infections and COVID-19

Fig. 2

Epigenetics in COVID-19 immune syndrome and targeted therapies. Cytokine storm occurred in the majority of severe COVID-19 cases; hypercytokinemia post-coronavirus infections can be harmful and sometimes deadly. Activated immune cells (T cells, DCs, macrophages, and neutrophils) act as the main immunity system performers. Main pro-inflammatory cytokines (IL-1β, IL-6, IL-12, TNF-α) and chemokines (CCL2, CCL3, CCL5, CXCL8, CXCL9, CXCL10) are upregulated by effector cells due to hyper-methylation and acetylation modifications taking place on histone marks. The increase in repressive histone mark led to a decrease in IL-12 and IL-1β. Epigenetic interventions such as HDACi, HATi, and DNMTi targeted both pro-inflammatory and anti-inflammatory cytokines (IL-10 and TGF-β). The ultimate goal of such interventions is to upregulate anti-inflammatory cytokines and to deplete pro-inflammatory cytokines’ levels through epigenetic modulation

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