Tags

Type your tag names separated by a space and hit enter

Role of pathogenic T cells and autoantibodies in relapse and progression of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis in LEW.1AV1 rats.
Immunology. 2009 Sep; 128(1 Suppl):e250-61.I

Abstract

Accumulating evidence suggests that T cells and autoantibodies reactive with myelin oligodendrocyte glycoprotein (MOG) play a critical role in the pathogenesis of multiple sclerosis (MS). In the present study, we have tried to elucidate the pathomechanisms of development and progression of the disease by analysing T cells and autoantibodies in MOG-induced rat experimental autoimmune encephalomyelitis (EAE), which exhibits various clinical subtypes mimicking MS. Analysis using overlapping peptides revealed that encephalitogenic epitopes resided in peptide 7 (P7, residue 91-108) and P8 (residue 103-125) of MOG. Immunization with MOGP7 and MOGP8 induced relapsing-remitting or secondary progressive EAE. T cells taken from MOG-immunized and MOGP7-immunized rats responded to MOG and MOGP7 and sera from MOG-immunized rats reacted to MOG and MOGP1. Significant epitope spreading was not observed at either T-cell or antibody levels. Interestingly, sera from MOGP7-immunized rats with clinical signs did not react to MOG and MOG peptides throughout the observation period, suggesting that disease development and relapse in MOGP7-induced EAE occur without autoantibodies. However, MOGP7 immunization with adoptive transfer of anti-MOG antibodies aggravated the clinical course of EAE only slightly. Analysis of antibodies against conformational epitope (cme) suggests that anti-MOG(cme) may play a role in the pathogenicity of anti-MOG antibodies. Collectively, these findings demonstrated that relapse of a certain type of MOG-induced EAE occurs without autoantibodies but that autoantibodies may play a role in disease progression. Relapses and the progression of MS-mimicking EAE are differently immunoregulated so immunotherapy should be designed appropriately on the basis of precise information.

Authors+Show Affiliations

Department of Molecular Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan. matyoh@tmin.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19175799

Citation

Matsumoto, Yoh, et al. "Role of Pathogenic T Cells and Autoantibodies in Relapse and Progression of Myelin Oligodendrocyte Glycoprotein-induced Autoimmune Encephalomyelitis in LEW.1AV1 Rats." Immunology, vol. 128, no. 1 Suppl, 2009, pp. e250-61.
Matsumoto Y, Park IK, Hiraki K, et al. Role of pathogenic T cells and autoantibodies in relapse and progression of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis in LEW.1AV1 rats. Immunology. 2009;128(1 Suppl):e250-61.
Matsumoto, Y., Park, I. K., Hiraki, K., Ohtani, S., & Kohyama, K. (2009). Role of pathogenic T cells and autoantibodies in relapse and progression of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis in LEW.1AV1 rats. Immunology, 128(1 Suppl), e250-61. https://doi.org/10.1111/j.1365-2567.2008.02955.x
Matsumoto Y, et al. Role of Pathogenic T Cells and Autoantibodies in Relapse and Progression of Myelin Oligodendrocyte Glycoprotein-induced Autoimmune Encephalomyelitis in LEW.1AV1 Rats. Immunology. 2009;128(1 Suppl):e250-61. PubMed PMID: 19175799.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of pathogenic T cells and autoantibodies in relapse and progression of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis in LEW.1AV1 rats. AU - Matsumoto,Yoh, AU - Park,Il-Kwon, AU - Hiraki,Keiko, AU - Ohtani,Shin, AU - Kohyama,Kuniko, Y1 - 2008/10/29/ PY - 2009/1/30/entrez PY - 2009/1/30/pubmed PY - 2010/1/26/medline SP - e250 EP - 61 JF - Immunology JO - Immunology VL - 128 IS - 1 Suppl N2 - Accumulating evidence suggests that T cells and autoantibodies reactive with myelin oligodendrocyte glycoprotein (MOG) play a critical role in the pathogenesis of multiple sclerosis (MS). In the present study, we have tried to elucidate the pathomechanisms of development and progression of the disease by analysing T cells and autoantibodies in MOG-induced rat experimental autoimmune encephalomyelitis (EAE), which exhibits various clinical subtypes mimicking MS. Analysis using overlapping peptides revealed that encephalitogenic epitopes resided in peptide 7 (P7, residue 91-108) and P8 (residue 103-125) of MOG. Immunization with MOGP7 and MOGP8 induced relapsing-remitting or secondary progressive EAE. T cells taken from MOG-immunized and MOGP7-immunized rats responded to MOG and MOGP7 and sera from MOG-immunized rats reacted to MOG and MOGP1. Significant epitope spreading was not observed at either T-cell or antibody levels. Interestingly, sera from MOGP7-immunized rats with clinical signs did not react to MOG and MOG peptides throughout the observation period, suggesting that disease development and relapse in MOGP7-induced EAE occur without autoantibodies. However, MOGP7 immunization with adoptive transfer of anti-MOG antibodies aggravated the clinical course of EAE only slightly. Analysis of antibodies against conformational epitope (cme) suggests that anti-MOG(cme) may play a role in the pathogenicity of anti-MOG antibodies. Collectively, these findings demonstrated that relapse of a certain type of MOG-induced EAE occurs without autoantibodies but that autoantibodies may play a role in disease progression. Relapses and the progression of MS-mimicking EAE are differently immunoregulated so immunotherapy should be designed appropriately on the basis of precise information. SN - 1365-2567 UR - https://www.unboundmedicine.com/medline/citation/19175799/Role_of_pathogenic_T_cells_and_autoantibodies_in_relapse_and_progression_of_myelin_oligodendrocyte_glycoprotein_induced_autoimmune_encephalomyelitis_in_LEW_1AV1_rats_ L2 - https://doi.org/10.1111/j.1365-2567.2008.02955.x DB - PRIME DP - Unbound Medicine ER -