Epstein-Barr virus latent membrane protein 2A exacerbates experimental autoimmune encephalomyelitis and enhances antigen presentation function

Sci Rep. 2012:2:353. doi: 10.1038/srep00353. Epub 2012 Apr 3.

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Antigen Presentation / drug effects
  • Antigen Presentation / immunology*
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • Cell Proliferation / drug effects
  • Cytokines / immunology
  • Cytokines / metabolism
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Encephalomyelitis, Autoimmune, Experimental / pathology
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Flow Cytometry
  • Humans
  • Immunoglobulin G / immunology
  • Immunoglobulin G / metabolism
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / immunology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Molecular Sequence Data
  • Myelin-Oligodendrocyte Glycoprotein / genetics
  • Myelin-Oligodendrocyte Glycoprotein / immunology
  • Myelin-Oligodendrocyte Glycoprotein / pharmacology
  • Peptide Fragments / genetics
  • Peptide Fragments / immunology
  • Peptide Fragments / pharmacology
  • Severity of Illness Index
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • Viral Matrix Proteins / genetics
  • Viral Matrix Proteins / immunology*
  • Viral Matrix Proteins / metabolism

Substances

  • Cytokines
  • EBV-associated membrane antigen, Epstein-Barr virus
  • Immunoglobulin G
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments
  • Viral Matrix Proteins
  • myelin oligodendrocyte glycoprotein (35-55)