Myelin-specific T cells in animals with Japanese macaque encephalomyelitis

Aparna N Govindan1, Kristin S Fitzpatrick1, Minsha Manoharan1

  • 1Vaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton, OR, USA.

Abstract

Insights

Japanese macaque encephalomyelitis (JME) involves myelin-specific T cells in the central nervous system and periphery. These findings offer insights into inflammatory demyelinating disease pathogenesis potentially linked to gamma-herpesvirus infection.

Area of Science:

  • Neuroimmunology
  • Veterinary Neurology
  • Demyelinating Diseases

Background:

  • Japanese macaque encephalomyelitis (JME) is a spontaneous demyelinating disease in macaques, serving as a model for multiple sclerosis (MS).
  • Understanding the immunological underpinnings of JME is crucial for elucidating inflammatory demyelinating disease pathogenesis.

Purpose of the Study:

  • To investigate the presence and characteristics of myelin-specific T cells in the central nervous system (CNS) and periphery of Japanese macaques with JME.
  • To explore the role of T-cell responses, including CD4+ and CD8+ T cells, and cytokine expression (IL-17, IFNγ) in JME pathogenesis.

Main Methods:

  • Analysis of mononuclear cells (MNCs) from CNS lesions, cervical lymph nodes (LNs), and peripheral blood of JME-affected and control macaques.
  • Detection of myelin-specific T cells targeting myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), and proteolipid protein (PLP).
  • Assessment of T-cell responses (CD4+, CD8+, Th1, Th17) and cytokine expression (IL-17, IFNγ).

Main Results:

  • Demyelinating JME lesions contained CD4+ and CD8+ T cells specific for MOG, MBP, and PLP.
  • CD8+ T-cell responses were absent in JME peripheral blood, but CD4+ Th1 and Th17 responses were detected.
  • Cervical LN MNCs from most JME animals showed myelin-specific T cells not found in controls.
  • Sequence analysis revealed similarities between myelin antigens and JM rhadinovirus (JMRV) open reading frames.

Conclusions:

  • JME exhibits an immune-mediated component involving myelin-specific CD4+ and CD8+ T cells.
  • JME pathogenesis may be linked to gamma-herpesvirus infection, offering insights into inflammatory demyelinating diseases.