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Author Spotlight: Creating a Versatile Experimental Autoimmune Encephalomyelitis Model Relevant for Both Male and Female Mice
Published on: October 13, 2023
Immunopathology of Japanese macaque encephalomyelitis is similar to multiple sclerosis
Tiffany C Blair1, Minsha Manoharan1, Stephanie D Rawlings-Rhea1
1Vaccine and Gene Therapy Institute, Oregon Health & Science University (OHSU), 505 NW 185th Avenue, Beaverton, OR 97006, United States.
Abstract:
Japanese macaque encephalomyelitis (JME) is an inflammatory demyelinating disease that occurs spontaneously in a colony of Japanese macaques (JM) at the Oregon National Primate Research Center. Animals with JME display clinical signs resembling multiple sclerosis (MS), and magnetic resonance imaging reveals multiple T2-weighted hyperintensities and gadolinium-enhancing lesions in the central nervous system (CNS). Here we undertook studies to determine if JME possesses features of an immune-mediated disease in the CNS. Comparable to MS, the CNS of animals with JME contain active lesions positive for IL-17, CD4+ T cells with Th1 and Th17 phenotypes, CD8+ T cells, and positive CSF findings.
Insights
Japanese macaque encephalomyelitis (JME) is an inflammatory brain disease in macaques resembling multiple sclerosis. Studies indicate JME is immune-mediated, with active lesions in the central nervous system showing inflammatory markers.
Area of Science:
- Neuroimmunology
- Comparative Pathology
- Primate Models
Background:
- Japanese macaque encephalomyelitis (JME) is a spontaneous inflammatory demyelinating disease in Japanese macaques (JM).
- Clinical and MRI findings in JME resemble human multiple sclerosis (MS).
Purpose of the Study:
- To investigate if JME exhibits characteristics of an immune-mediated central nervous system (CNS) disease.
- To compare the immunological features of JME lesions with those of MS.
Main Methods:
- Analysis of CNS lesions in JME-affected macaques.
- Immunohistochemical staining for inflammatory markers (IL-17, T cell subsets).
- Cerebrospinal fluid (CSF) analysis.
Main Results:
- JME lesions showed positive staining for IL-17.
- Active lesions contained CD4+ T cells with Th1 and Th17 phenotypes, and CD8+ T cells.
- CSF findings were consistent with an inflammatory CNS process.
Conclusions:
- JME shares key immunological features with immune-mediated CNS diseases like MS.
- The presence of specific T cell subsets and inflammatory markers supports an immune-mediated etiology for JME.
- JME serves as a relevant preclinical model for studying immune-mediated demyelinating diseases.
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