Creation of a model for multiple sclerosis in Callithrix jacchus marmosets

Multiple sclerosis (MS) is an inflammatory disease of the CNS white matter characterized pathologically by the accumulation of perivascular and parenchymal T lymphocytes (T cells), and macrophage infiltration associated with myelin destruction. MS lesions are also characterized by the death of oligo...

Full description

Saved in:
Bibliographic Details
Published in:Journal of molecular medicine (Berlin, Germany) Germany), 1997-03, Vol.75 (3), p.187-197
Main Authors: GENAIN, C. P, HAUSER, S. L
Format: Article
Language:English
Subjects:
Adoptive Transfer
Animals
Biological and medical sciences
Callithrix
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental - etiology
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - pathology
Humans
Immunization
Medical sciences
Multiple Sclerosis
Myelin Proteins - immunology
Neurology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Multiple sclerosis (MS) is an inflammatory disease of the CNS white matter characterized pathologically by the accumulation of perivascular and parenchymal T lymphocytes (T cells), and macrophage infiltration associated with myelin destruction. MS lesions are also characterized by the death of oligodendrocytes (the myelin-producing cells) and proliferation and hypertrophy of astrocytes with scar tissue (gliosis) replacing normal myelin. These changes result in the loss of axonal conduction for neurons of the CNS and in clinical disability. MS is thought to be an autoimmune disease, in particular because of its analogy with the disease model of experimental allergic encephalomyelitis (EAE). Despite extensive research and the availability of various EAE models in laboratory rodents the etiology of human MS has not been identified, and to date no effective treatment exists. Phylogenetic differences may limit the usefulness of existing EAE models, and indeed no single form of rodent EAE recapitulates all the clinical and pathological features of MS. Here we describe a novel form of EAE created in a nonhuman primate, the common marmoset Callithrix jacchus. Active immunization of these monkeys with whole myelin produces a primary demyelinating disease with a chronic relapsing-remitting course, characterized pathologically by moderate inflammation with prominent and early demyelination and gliosis reminiscent of human MS. Adoptive and passive transfer experiments have permitted definition of the mechanisms responsible for the MS-like pathology. Production of the fully demyelinated lesion requires synergism between encephalitogenic (e.g., disease-inducing) T cells and pathogenic antibody. The antigens of myelin that promote encephalitogenic T cell and antibody responses in this system have been identified. Because of the similarity between the two conditions and the high degree of conservation in immune and nervous system genes between nonhuman primates and humans, future studies of marmoset EAE will likely accelerate the development of therapies for human MS.
ISSN:0946-2716
1432-1440
DOI:10.1007/s001090050103