New research by Johns Hopkins researchers finds that neutrophils — front-line immune cells essential to fighting infections — may be altered by SARS-CoV-2, the virus that causes COVID-19, to cease their normal function of destroying pathogens in the body and, instead, significantly inhibit other immune cells critical for fighting the virus.

The team says their finding, published in Science Translational Medicine, could help explain a mechanism by which severe COVID may arise.

“Our findings suggest that in some COVID infections, SARS-CoV-2 may dramatically impair the immune response by reprogramming neutrophils into a cell type called polymorphonuclear myeloid-derived suppressor cells, or PMN-MDSCs,” which are known to suppress virus-fighting T cells, says study senior author Andrea Cox, Johns Hopkins professor of medicine and oncology.

Better understanding the mechanism for neutrophil conversion into PMN-MDSCs may lead to new therapy options for severe COVID, says Cox. In fact, she explains, a potential treatment might already exist.

Antibodies against PD–L1, a key protein known to negatively affect the immune system, have been used to treat cancers, she notes, so the team tried adding them in the lab to neutrophils co-cultured with SARS-CoV-2.

“T-cell suppression was reduced, and T-cell activity — marked by the release of cytokines — increased; therefore, PD-L1 antibodies may provide a means of treating people with severe COVID in combination with antiviral medications or as a stand-alone therapy when a patient is unable to take antiviral medications,” Cox says.