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

7Citations
Citations of this article
28Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Abstract: 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. Highlights: Latent form of EBV potentially triggers autoimmune diseasesABCs expand in autoimmunity and contribute to disease pathogenesisEBV modifies ABCs, so as to function pathogenically in autoimmune diseasesApart from EBV elimination, targeting of ABCs may also bring therapeutic benefits to autoimmune patients

Cite

CITATION STYLE

APA

Sachinidis, A., & Garyfallos, A. (2022, August 1). Involvement of age-associated B cells in EBV-triggered autoimmunity. Immunologic Research. Springer. https://doi.org/10.1007/s12026-022-09291-y

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free