Study links SARS-CoV-2 autoantibodies to B-cell dysregulation

A study published in the journal Immunity by Yuan et al. has identified a link between SARS-CoV-2 infections and the development of autoantibodies due to B-cell dysregulation. By analyzing blood samples from patients 3 to 58 days after the onset of symptoms using single-cell RNA and ATAC sequencing, researchers identified a specific subset of immune cells driving this process.

The study highlights the role of atypical memory B cells (B AM) that are T-bet-positive and CD11c-positive. These cells exhibit characteristics similar to those found in patients with systemic lupus erythematosus (SLE) and show low somatic hypermutation, suggesting they have not completed the standard maturation process.

Patients with high plasma autoantibody levels also demonstrated higher markers for Type-III interferon activity and B-cell proliferation. Notably, during the convalescence phase, these individuals showed lower levels of SARS-CoV-2 neutralizing antibodies. The research suggests that this immune system malfunction occurs independently of viral load or general inflammatory and tissue damage markers.