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Critical role of antigen-specific antibody in experimental autoimmune encephalomyelitis induced by recombinant myelin oligodendrocyte glycoprotein.
Eur J Immunol. 2002 Jul; 32(7):1905-13.EJ

Abstract

The role of B cells and antibody in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) remains controversial. We previously demonstrated that B cells are required for EAE to be induced by the 120-amino acid extracellular domain of myelin oligodendrocyte glycoprotein (MOG). In the present study, the role of B cells in MOG-induced EAE was further characterized. Passive transfer of activated B cells or serum from MOG-primed wild-type (WT) mice was found to reconstitute the ability for clinical and histological EAE to be induced in MOG-immunized B cell-deficient mice. MOG-induced EAE did not occur with transfer of B cells that had been nonspecifically activated by lipopolysaccharide or isolated from naïve or myelin basic protein (MBP)-primed WT mice. Likewise, MOG-primed serum, but not naive serum or serum from MBP-, Hen egg lysozyme-, or MOG(35-55)-primed mice, led to EAE in B cell-/- animals. While both MOG-primed B cells and serum reconstituted the ability for disease induction, MOG-primed serum was much more efficient, leading to clinical and histological EAE similar to that seen in the WT. Injection of MOG serum into healthy B cell-/- mice 30 days after MOG immunization led to rapid appearance of clinical signs and CNS inflammation, indicating that an antigen-specific factor is necessary for initiation of CNS inflammation,and not just demyelination. These data strongly suggest that MOG-specific antibody is critical to the initiation of MOG-induced murine EAE.

Authors+Show Affiliations

Department of Neurology and Neurosurgery, Washington University School of Medicine, Saint Louis, MO 63110, USA. lyonsj@neuro.wustl.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

12115610

Citation

Lyons, Jeri-Anne, et al. "Critical Role of Antigen-specific Antibody in Experimental Autoimmune Encephalomyelitis Induced By Recombinant Myelin Oligodendrocyte Glycoprotein." European Journal of Immunology, vol. 32, no. 7, 2002, pp. 1905-13.
Lyons JA, Ramsbottom MJ, Cross AH. Critical role of antigen-specific antibody in experimental autoimmune encephalomyelitis induced by recombinant myelin oligodendrocyte glycoprotein. Eur J Immunol. 2002;32(7):1905-13.
Lyons, J. A., Ramsbottom, M. J., & Cross, A. H. (2002). Critical role of antigen-specific antibody in experimental autoimmune encephalomyelitis induced by recombinant myelin oligodendrocyte glycoprotein. European Journal of Immunology, 32(7), 1905-13.
Lyons JA, Ramsbottom MJ, Cross AH. Critical Role of Antigen-specific Antibody in Experimental Autoimmune Encephalomyelitis Induced By Recombinant Myelin Oligodendrocyte Glycoprotein. Eur J Immunol. 2002;32(7):1905-13. PubMed PMID: 12115610.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Critical role of antigen-specific antibody in experimental autoimmune encephalomyelitis induced by recombinant myelin oligodendrocyte glycoprotein. AU - Lyons,Jeri-Anne, AU - Ramsbottom,Michael J, AU - Cross,Anne H, PY - 2002/7/13/pubmed PY - 2002/8/14/medline PY - 2002/7/13/entrez SP - 1905 EP - 13 JF - European journal of immunology JO - Eur J Immunol VL - 32 IS - 7 N2 - The role of B cells and antibody in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) remains controversial. We previously demonstrated that B cells are required for EAE to be induced by the 120-amino acid extracellular domain of myelin oligodendrocyte glycoprotein (MOG). In the present study, the role of B cells in MOG-induced EAE was further characterized. Passive transfer of activated B cells or serum from MOG-primed wild-type (WT) mice was found to reconstitute the ability for clinical and histological EAE to be induced in MOG-immunized B cell-deficient mice. MOG-induced EAE did not occur with transfer of B cells that had been nonspecifically activated by lipopolysaccharide or isolated from naïve or myelin basic protein (MBP)-primed WT mice. Likewise, MOG-primed serum, but not naive serum or serum from MBP-, Hen egg lysozyme-, or MOG(35-55)-primed mice, led to EAE in B cell-/- animals. While both MOG-primed B cells and serum reconstituted the ability for disease induction, MOG-primed serum was much more efficient, leading to clinical and histological EAE similar to that seen in the WT. Injection of MOG serum into healthy B cell-/- mice 30 days after MOG immunization led to rapid appearance of clinical signs and CNS inflammation, indicating that an antigen-specific factor is necessary for initiation of CNS inflammation,and not just demyelination. These data strongly suggest that MOG-specific antibody is critical to the initiation of MOG-induced murine EAE. SN - 0014-2980 UR - https://www.unboundmedicine.com/medline/citation/12115610/Critical_role_of_antigen_specific_antibody_in_experimental_autoimmune_encephalomyelitis_induced_by_recombinant_myelin_oligodendrocyte_glycoprotein_ L2 - https://doi.org/10.1002/1521-4141(200207)32:7<1905::AID-IMMU1905>3.0.CO;2-L DB - PRIME DP - Unbound Medicine ER -