Abstract
Hyperactivation of the immune response, including release of pro-inflammatory cytokines such as interleukin-6 (IL-6), might play a key role in the pathophysiology of severe illness from COVID-19.1 Consistent with this notion, one of the few therapies that reduces mortality in hospitalised patients with COVID-19 is the corticosteroid, dexamethasone.2 Accordingly, there has been great interest in examining whether treatment with additional, more targeted anti-inflammatory agents beyond steroids could provide further benefit.
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