Study Probes Why Autoantibodies Are Produced in Some COVID Patients

The autoantibodies are triggered in a way that is similar to other autoimmune diseases, like lupus.

Sept. 3, 2026

Key Highlights

- The study analyzed data from 209 COVID-19 patients, focusing on differences in autoantibody levels among women.
- Higher levels of atypical memory B cells, especially DN2 subtypes, were linked to increased autoantibody production in some patients.
- Findings suggest SARS-CoV-2 can activate immune pathways similar to those involved in autoimmune diseases, potentially explaining post-infection autoimmune symptoms.
- The research provides insight into immune cell behavior that may underlie persistent symptoms and autoimmune risks following COVID-19.
- Understanding these mechanisms could inform future treatments to prevent or mitigate autoimmune complications after viral infections.

A new study in Immunity investigates why autoantibodies (Abs) are produced in some COVID-19 patients. CIDRAP has the news.

Autoantibodies are proteins that mistakenly target the body’s own tissues instead of finding and destroying illness-causing invaders. They are linked to severe illness, persistent symptoms, and an increased risk of new-onset autoimmune disease in some COVID-infected people.

The researchers for the study analyzed data from 209 COVID-infected participants, and eventually selected 12 age-matched women with different autoantibody levels. They were separated into a low autoantibody group (autoAb-low) and a high one (autoAb-high). A subset of immune cells known as atypical memory B cells were more likely to develop into autoantibody-secreting cells in participants in the autoAb-high group than in those in the autoAb-low group.

A subtype of atypical memory B cells known as double-negative 2 (DN2) B cells were also overrepresented in the high-autoantibody group. DN2 cells have been linked to autoantibody production and may play a role in other autoimmune diseases like lupus.

The study’s lead author suggests that “SARS-CoV-2 infection can activate an immune program that closely resembles those involved in established autoimmune disorders, helping explain why some individuals experience autoimmune complications following infection.”