Researchers at Michigan Medicine have discovered another functional autoantibody in COVID-19 patients that contributes to the disease’s development and the “firestorm” of blood clots and inflammation it induces. The autoantibody makes it harder for the body to degrade neutrophil extracellular traps, the toxic webs of DNA and proteins produced by overactive immune cells at heightened levels in COVID patients.
Inhibiting IRE1α, a molecule activated by the endoplasmic reticulum in neutrophils, counters disease progression in lupus mice.
An overactive defense response may lead to increased blood clotting, disease severity, and death from COVID-19. A phenomenon called NETosis—in which infection-fighting cells emit a web-like substance to trap invading viruses—is part of an immune response that becomes increasingly hyperactive in people on ventilators and people who die from the disease.