In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses

J Neuroimmunol. 2014 Jan 15;266(1-2):49-55. doi: 10.1016/j.jneuroim.2013.09.022. Epub 2013 Oct 5.

Abstract

F1 (SJL/J×C57BL/6) mice with MOG35-55-induced EAE recover from disease when treated with Ig-MOG carrying MOG35-55 peptide. However, Ig-PLP1, carrying PLP139-151, induced reduction of anti-MOG antibodies and exacerbated EAE. Herein, we show that Ig-PLP1 specifically reduces the frequency of B cells producing protective IgG2a/b anti-MOG antibodies. Surprisingly, these cells were marginal zone (MZ), rather than follicular (FO) or newly formed (NF), B cells and transfer of MZ B cells into sick mice nullified disease exacerbation by Ig-PLP1 in a complement dependent manner. These findings reveal a potential self-limiting regulatory mechanism involving auto-antibodies in MOG EAE.

Keywords: Anti-MOG antibodies; Autoimmunity; B cells; EAE; T cell tolerance.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies / metabolism
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • Cytokines / metabolism
  • Disease Models, Animal
  • Encephalomyelitis, Autoimmune, Experimental / chemically induced
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Encephalomyelitis, Autoimmune, Experimental / therapy*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Flow Cytometry
  • Immune Tolerance / physiology*
  • Lymphocyte Activation / immunology
  • Mice
  • Mice, Inbred C57BL
  • Myelin-Oligodendrocyte Glycoprotein / adverse effects
  • Peptide Fragments / adverse effects
  • Statistics, Nonparametric
  • T-Lymphocytes / immunology*

Substances

  • Antibodies
  • Cytokines
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments
  • myelin oligodendrocyte glycoprotein (35-55)