A team of researchers, partially supported by the NHLBI, have discovered autoantibodies in patients with COVID-19 that appear to contribute to severe inflammation and blood clotting. The findings, published in JCI Insight, may inform research to support the development of tailored COVID-19 therapies.
Neutrophils or white blood cells respond to foreign immune threats, including the virus that causes COVID-19, in many ways, including a process of casting spider web-like nets, called neutrophil extracellular traps (NETs), to trap pathogens and coordinate processes to clear out potentially dangerous debris (NETosis). Researchers have found autoantibodies can confuse these efforts and correlate with severe illness. In this paper, researchers describe immune activity from 328 patients hospitalized for COVID-19 in comparison to 48 healthy controls. They found COVID-19 patients with higher levels of the autoantibodies that prevent NETosis were more likely to have higher levels of inflammation and require breathing support.
As researchers study this dysregulated immune response in COVID-19, they are also finding similarities with other conditions, like cancer, lupus, and antiphospholipid syndrome (APS), a rare autoimmune disorder that results in antibodies attacking fat in cells, which can lead to blood clots and seizures. Yogen Kanthi, M.D., a study author and cardiologist and vascular medicine specialist at NHLBI, explains that in COVID-19 and APS, the anti-NET autoantibodies coat the surface of NETs, making it much harder for the body to clear out this web that causes inflammation and clotting. “Knowing their function is likely to help physicians design more targeted COVID-19 treatments and also for other inflammatory diseases,” he said.