Abstract
Multiple sclerosis (MS) is an inflammatory, autoimmune disease of the central nervous system. The cause of MS is still unknown but epidemiological and immunological studies have implicated Epstein-Barr virus (EBV), which infects B cells, as a possible etiological agent involved in disease. Of particular interest is EBV latent membrane protein 2A (LMP2A) because previous studies have demonstrated that LMP2A enhances the expansion and differentiation of B cells upon antigen stimulation, revealing a potential contribution of this protein in autoimmunity. Since B cells are thought to contribute to MS, we examined the role of LMP2A in the animal model experimental autoimmune encephalomyelitis (EAE). In this model, transgenic mice in which B cells express LMP2A show increased severity and incidence of disease. This difference was not due to lymphocyte recruitment into the CNS or differences in T cell activation, rather, we show that LMP2A enhances antigen presentation function.
| Original language | English (US) |
|---|---|
| Article number | 353 |
| Journal | Scientific reports |
| Volume | 2 |
| DOIs | |
| State | Published - 2012 |
Funding
RL is the Dan and Bertha Spear Research Professor and is supported by the Public Health Service grants CA133063 and CA73507 from the National Cancer Institute. SDM is the Judy Gugenheim Research Professor and is supported by grants NS-026543 and NS062365 from the National Institutes of Health. We would like to thank members of the Longnecker and Miller laboratory for help in the completion of these studies, in addition to Michelle Swanson-Mungerson and Melissa Brown for review of this manuscript. MOGBCR (IgH) mice were kindly provided by the Kuchroo laboratory (Harvard Medical School). E. coli expressing human rMOG protein were kindly provided by the Ruddle laboratory (Yale University School of Medicine).
ASJC Scopus subject areas
- General