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Anergy induction in encephalitogenic t-cells by brain microvessel endothelial-cells is inhibited by interleukin-1

Academic Article
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Overview

authors

  • Bourdoulous, S.
  • Beraud, E.
  • Lepage, C.
  • Zamora, A. J.
  • Ferry, A.
  • Bernard, D.
  • Strosberg, Donny
  • Couraud, P. O.

publication date

  • May 1995

journal

  • European Journal of Immunology  Journal

abstract

  • Experimental autoimmune encephalomyelitis (EAE) is an inflammatory disease of the central nervous system (CNS) which can be induced, in susceptible strains like Lewis rats, by transfer of activated myelin basic protein (MBP)-specific CD4+ T lymphocytes. The role of cerebral endothelium in the onset of EAE, with regard to adhesion, activation and infiltration in the CNS of encephalitogenic T lymphocytes, is not fully understood. When pretreated by interferon-gamma, the immortalized Lewis rat brain microvessel endothelial (RBE4) cells expressed major histocompatibility complex class II molecules and stimulated MBP-specific proliferation and cytolytic activity of the syngeneic encephalitogenic T cell line, designated PAS. However, RBE4-stimulated PAS lymphocytes subsequently entered an unresponsive state, known as anergy. When inoculated in syngeneic animals, anergic PAS cells, although still cytotoxic, failed to induce EAE, and no cell infiltration was detectable within CNS. The addition of interleukin-1 beta (IL-1 beta) during MBP presentation by RBE4 cells prevented T cell anergy induction, and maintained T cell encephalitogenicity, although PAS cells stimulated in these conditions caused delayed and attenuated clinical signs of EAE, with only discrete inflammatory lesions in the CNS, compared with EAE induced by PAS cells fully activated by thymic cells. Altogether, our results indicate that MBP presentation by brain microvessel endothelial cells to encephalitogenic T cells induces T cell anergy and loss of pathogenicity. In addition, IL-1 beta co-stimulation of T cells prevents anergy induction in vitro and at least partially maintains encephalitogenicity in vivo.

subject areas

  • Animals
  • Antigen Presentation
  • Base Sequence
  • Brain
  • Capillaries
  • Cell Adhesion
  • Cell Line, Transformed
  • Encephalomyelitis, Autoimmune, Experimental
  • Endothelium, Vascular
  • Guinea Pigs
  • Histocompatibility Antigens Class II
  • Humans
  • Immune Tolerance
  • Immunotherapy, Adoptive
  • Interferon-gamma
  • Interleukin-1
  • Interleukin-2
  • Interleukin-6
  • Lymphocyte Activation
  • Mice
  • Molecular Sequence Data
  • Myelin Basic Protein
  • Rats
  • Rats, Inbred Lew
  • Receptors, Interleukin-2
  • Recombinant Proteins
  • T-Lymphocytes, Cytotoxic
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Research

keywords

  • ANERGY
  • BRAIN ENDOTHELIUM
  • EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
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Identity

International Standard Serial Number (ISSN)

  • 0014-2980

Digital Object Identifier (DOI)

  • 10.1002/eji.1830250507

PubMed ID

  • 7539749
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Additional Document Info

start page

  • 1176

end page

  • 1183

volume

  • 25

issue

  • 5

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