Research ArticleCORONAVIRUS

Inhibition of Bruton tyrosine kinase in patients with severe COVID-19

See allHide authors and affiliations

Science Immunology  05 Jun 2020:
Vol. 5, Issue 48, eabd0110
DOI: 10.1126/sciimmunol.abd0110

Taming cytokine storm

Hyperactivation of immune cells leading to “cytokine storm” contributes to acute lung injury in patients with COVID-19 pneumonia. Host signaling proteins and effector molecules contributing to cytokine storm are potential targets for pharmacotherapy of COVID-19. Roschewski et al. conducted an observational study evaluating off-label use of acalabrutinib, an inhibitor of the Bruton tyrosine kinase (BTK) enzyme, in 19 hospitalized COVID-19 patients requiring oxygen supplementation. Biomarkers of inflammation reverted toward normal in most treated patients. Correlative studies of blood monocytes from patients with severe COVID-19 showed increases in BTK activation and production of interleukin-6, a key driver of cytokine storm, compared with healthy control monocytes. These findings helped inform the design of a randomized controlled clinical trial to further test the therapeutic potential of acalabrutinib in COVID-19.

This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

View Full Text

Stay Connected to Science Immunology