A major shortcoming of vaccines against COVID-19 and certain other microbial diseases is that the protection they offer is relatively brief—a matter of a few months. In research published online on January 11 in The Journal of Immunology, David R. Fooksman, PhD, Associate Professor, Pathology and Microbiology and Immunology, Albert Einstein College of Medicine, and colleagues report that inflammation may be a key reason.
Infection and vaccinations stimulate the formation of antibody-secreting cells (ASCs)—crucial “memory cells” that continuously secrete antibodies against reinfection by a particular microbe. Until now, ASCs were thought to be immotile cells, secreting antibodies from niches in the bone marrow. In experiments involving mice, the researchers found that the inflammatory cytokine tumor necrosis factor alpha (TNF-α) can rapidly (within hours) disrupt ASC survival in the bone marrow in two ways: by causing ASCs to migrate from their bone-marrow niches into the bloodstream and by preventing new ASCs from getting into the bone marrow from the blood.
The findings may explain how major inflammatory events, including cytokine storms and infections, can diminish previously existing ASCs and the serological (antibody-related) memory they provide.
