Pathogenic and regulatory roles for B cells in experimental autoimmune encephalomyelitis

Abstract

A dual role of B cells in experimental autoimmune encephalomyelitis (EAE), the animal model of the human autoimmune disease multiple sclerosis (MS), has been established. In the first role, B cells contribute to the pathogenesis of EAE through the production of anti-myelin antibodies that contribute to demyelination. On the contrary, B cells have also been shown to have protective functions in that they play an essential role in the spontaneous recovery from EAE. In this review, we summarize studies conducted in a number of species demonstrating the conditions under which B cells are pathogenic in EAE. We also discuss the phenotype and anti-inflammatory mechanisms of regulatory B cells.

Keywords::

• B cell
• experimental autoimmune encephalomyelitis
• immune regulation
• immunoglobulin
• multiple sclerosis

Acknowledgements

The authors thank Dr. Mark Shlomchik, Yale University, New Haven, CT for providing the Vh186.2 mice. We also thank Dr. Eugene Ponomarev for technical assistance and Shelley Morris for assistance with the mice. This work was supported by grants from the National Multiple Sclerosis Society (RG 3299-A-2) and from the NIH, NIAID (R01 AI069358).

Declaration of interest: The authors report no conflicts of interests. The authors alone are responsible for the content and writing of the paper.