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Updated: Jul 9, 2026
Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis
Published on: October 13, 2023
Characterization of the encephalitogenic immune response in a model of multiple sclerosis
Katrien L de Graaf1, Silvia Barth, Martin M Herrmann
1Experimental Neuroimmunology Laboratory, Hertie Institute for Clinical Brain Research, Department of General Neurology, University of Tübingen, Tübingen, Germany.
Abstract:
Experimental autoimmune encephalomyelitis (EAE) can be actively induced with the extracellular domain of myelin oligodendrocyte glycoprotein (MOG 1-125). MOG-EAE closely mimics multiple sclerosis (MS) especially as far as demyelination, lesion formation and axonal pathology are concerned. MOG 91-108 is the encephalitogenic stretch within MOG 1-125 in two EAE-susceptible MHC congenic LEW rat strains [LEW.1AV1 (RT1(av1)) and LEW.1N (RT1(n))] and DA (RT1(av1)) rats. In LEW.1AV1 rats, disease could be induced with MOG 96-104 and to a lesser extent with MOG 98-106, whereas in LEW.1N rats, only MOG 98-106 was pathogenic. Both peptides bound well to their restricting MHC class II molecules, i.e., RT1.D(n) in the LEW.1N rat and RT1.B(a) in the LEW.1AV1 rat. TCR spectratyping of MOG 91-108 immunized LEW.1N, LEW.1AV1 and DA rats revealed that MHC class II determined the TCRBV preference of CNS infiltrating T cells. The data demonstrate that the most critical factor in inducing MS like pathology is presentation of autoantigenic peptides on MHC class II molecules resulting in demyelination and axonal pathology.
Insights
Experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), is induced by myelin oligodendrocyte glycoprotein (MOG) peptides. MHC class II molecules dictate the T-cell response, leading to demyelination and axonal damage in EAE.
Area of Science:
- Neuroimmunology
- Autoimmunity
- Molecular immunology
Background:
- Experimental autoimmune encephalomyelitis (EAE) serves as a crucial animal model for multiple sclerosis (MS).
- Myelin oligodendrocyte glycoprotein (MOG) is a key autoantigen in EAE, particularly its extracellular domain (MOG 1-125).
- Specific MOG peptide fragments, such as MOG 91-108, are identified as encephalitogenic in susceptible rat strains.
Purpose of the Study:
- To investigate the role of specific MOG peptide epitopes in EAE induction.
- To determine the influence of MHC class II molecules on T-cell receptor (TCR) usage in EAE.
- To elucidate the mechanisms underlying demyelination and axonal pathology in MOG-induced EAE.
Main Methods:
- Induction of EAE in LEW.1AV1, LEW.1N, and DA rats using MOG peptides (MOG 1-125, MOG 91-108, MOG 96-104, MOG 98-106).
- Analysis of peptide binding to relevant MHC class II molecules (RT1.D(n) and RT1.B(a)).
- TCR spectratyping of T cells infiltrating the central nervous system (CNS) in immunized rats.
Main Results:
- Different MOG peptide fragments (MOG 96-104, MOG 98-106) were pathogenic in specific rat strains (LEW.1AV1, LEW.1N).
- The encephalitogenic peptide MOG 91-108 induced EAE in multiple rat strains.
- MHC class II genotype significantly influenced the TCRBV repertoire of CNS-infiltrating T cells.
Conclusions:
- Autoantigenic peptide presentation by MHC class II molecules is critical for initiating MS-like pathology.
- MHC class II molecules dictate the TCR preference of T cells targeting the CNS.
- Understanding these interactions is key to developing targeted therapies for MS.
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