A new study pinpoints the type of immune cell that produces self attacking antibodies tied to severe COVID 19, Long COVID, and new onset autoimmune disease.
Researchers have identified a specific B cell population, and the molecular program driving it, as the source of the self-attacking antibodies (autoantibodies) linked to severe COVID-19, Long COVID, and new-onset autoimmune disease, according to a new study published in the journal Immunity.
The Institute for Systems Biology-led team worked with the INCOV longitudinal COVID-19 cohort and combined single-cell RNA sequencing, chromatin accessibility profiling, plasma proteomics, proteome-wide autoantibody profiling, and genetic analyses. That multi-omics integration moves the field beyond the prior statistical link between autoantibodies and severe disease: the work names a defined effector B cell subset and its regulatory program, giving researchers a concrete cellular handle on infection-driven autoimmunity.
The paper's own conclusion is restrained: the findings "provide insights into the molecular and genetic basis of infection-induced autoimmunity in COVID-19 and its downstream outcomes, including Long COVID." Senior author Jim Heath, PhD, ISB president and professor, has described the identified cell population as a candidate target for new therapies, not an imminent one.
What remains unknown is whether the same B cell program operates in other post-infectious autoimmune conditions, and whether it can be suppressed without compromising normal antibody defenses. The next milestone is independent replication in larger, more diverse cohorts.