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letter
. 2020 Jul 5;87(3):1578–1581. doi: 10.1111/bcp.14437

FIGURE 1.

FIGURE 1

T helper 17 (Th17) cells are differentiated from naïve precursor T cells in response to coronavirus presentation, after co‐stimulation by antigen presenting cells and transforming growth factor‐β (TGF‐β) secretion. Th17 cells produce interleukin‐17A (IL‐17A) causing wide spectrum cell activation (e.g., dendritic cells, endothelial cells and fibroblasts). IL‐17 contributes to cytokine release storm by stimulating excessive and uncontrolled production of proinflammatory interleukins (e.g., IL‐1β, IL‐6 and IL‐8), tumour necrosis factor‐alpha, colony stimulating factors and chemokines. Secukinumab and ixekizumab are immunomodulators that block IL‐17A and could be beneficial in therapy of severe COVID‐19. Brodalumab is directed against interleukin‐17 receptor A (IL‐17RA), another potential target molecule in therapy of severe COVID‐19. CCL20, chemokine CC motif ligand 20; CXCR2, CXC chemokine receptor 2; G‐CSF, granulocyte colonystimulating factor; GM‐CSF, granulocyte‐macrophage CSF; IL, interleukin; R, receptor; Th17 cells, T helper 17 cells; Treg, regulatory T cells; TGF‐β, transforming growth factor‐ β;TNF‐α, tumour necrosis factor‐alpha