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COVID-19 is instead characterised by circulating T cells that show an activated Th17 membrane phenotype (CD38+HLA-DR+CD4+CCR6+)4 and express granulocyte–macrophage colony-stimulating factor (GM-CSF) in part along with IFNγ. Concentrations of both IL-17 and IFNγ are increased in serum from patients with COVID-19 in proportion with viral load and lung injury

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Leronlimab downregulates CD4 cells, GM-CSF, IFNy and IL-17. The authors postulate that the main contributor to inflammatory effects may be IL-33. No problem leronlimab has that covered too. Extracellular ATP triggers the release of IL-33, CCR5 blockade of CCL5 downregulates extracellular ATP and in turn downregulates IL-33.

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Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded γδ T cells. In severe COVID-19 cases, the IL-33–ST2 axis might act to expand the number of pathogenic granulocyte–macrophage colony-stimulating factor-expressing T cells, dampen antiviral interferon responses, elicit hyperinflammation, and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial–mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target IL-33 (eg, anti-ST2), T helper 17-like γδ T cells, immune cell homing, and cytokine balance.

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