Involvement of age-associated B cells in EBV-triggered autoimmunity

EBV infection has long been suspected to play a role in the development of autoimmune diseases. Interestingly, a recently published study has provided the strongest evidence to date that EBV is truly a trigger for multiple sclerosis, a well known inflammatory and neurodegenerative autoimmune disorder. Taking into account the data derived from mice models of autoimmune diseases that were also infected with a murine analog of EBV, in this commentary, we highlight the involvement of age-associated B cells, a B cell population defined as CD19(+)CD11c(+)CD21(-)T-bet(+), in the process of EBV-triggered autoimmunity. Of note, the aforementioned B cell subset expands continuously with age in healthy individuals, whereas displays a premature strong accumulation in cases of autoimmune diseases. These cells contribute to autoimmune disease pathogenesis via a variety of functions, such as the production of autoantibodies and/or the formation of spontaneous germinal centers. Latent form of EBV seems to modify these B cells, so as to function pathogenically in cases of autoimmunity. Targeting of ABCs, as well as the elimination of EBV, may both be potential treatments for autoimmunity.

Automated summary

A recently published study has provided strong evidence that EBV is a trigger for multiple sclerosis. The involvement of age-associated B cells in EBV-triggered autoimmunity is highlighted, as they contribute to the pathogenesis of autoimmune diseases through various functions, such as autoantibody production and germinal center formation. Targeting these B cells and eliminating EBV may be potential treatments for autoimmunity.