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A comparative analysis of B cell-mediated myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis pathogenesis in B cell-deficient mice reveals an effect on demyelination.

Svensson, Lars LU ; Abdul-Majid, Khairul-Bariah; Bauer, Jan; Lassmann, Hans; Harris, Robert A and Holmdahl, Rikard LU (2002) In European Journal of Immunology 32(7). p.1939-1946
Abstract
We have investigated the role of B cells in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) using B cell-deficient mice muMT) and mice bearing the X-linked immunodeficiency (xid). The mice were immunized with MOG(1-125 )in complete Freund's adjuvant but without use of pertussis toxin. B cell-deficient muMT mice on different genetic backgrounds (C57BL/10 and DBA/1 strains) developed EAE, although with a reduced clinical severity. Histological analyses revealed decreased demyelination in the central nervous system while the influx of inflammatory cells was similar or only slightly reduced as compared to B cell-sufficient control mice. Xid mice on the DBA/1 background also developed disease... (More)
We have investigated the role of B cells in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) using B cell-deficient mice muMT) and mice bearing the X-linked immunodeficiency (xid). The mice were immunized with MOG(1-125 )in complete Freund's adjuvant but without use of pertussis toxin. B cell-deficient muMT mice on different genetic backgrounds (C57BL/10 and DBA/1 strains) developed EAE, although with a reduced clinical severity. Histological analyses revealed decreased demyelination in the central nervous system while the influx of inflammatory cells was similar or only slightly reduced as compared to B cell-sufficient control mice. Xid mice on the DBA/1 background also developed disease with a reduced disease severity. The anti-MOG antibody response in the xid mice was decreased, while the T cell response to MOG was unaffected. We thus demonstrate that B cells are not critical for the development of MOG-induced EAE but contribute to the severity. The contribution of B cells to pathogenesis appears to be mainly through demyelination rather than through inflammation. (Less)
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published
subject
keywords
Non-U.S. Gov't, Support, Rats, Myelin-Associated Glycoprotein : adverse effects, Myelin Sheath : metabolism, Inbred DBA, Mice, Inbred C57BL, Male, Immunologic Deficiency Syndromes, Female, Encephalomyelitis, Experimental Autoimmune : pathology, T-Lymphocytes : immunology, Experimental Autoimmune : chemically induced, Demyelinating Diseases, Comparative Study, Central Nervous System : pathology, B-Lymphocytes : immunology, Animal
in
European Journal of Immunology
volume
32
issue
7
pages
1939 - 1946
publisher
John Wiley & Sons
external identifiers
  • wos:000176855000016
  • pmid:12115614
  • scopus:0036318944
ISSN
1521-4141
DOI
10.1002/1521-4141(200207)32:7<1939::AID-IMMU1939>3.0.CO;2-S
language
English
LU publication?
yes
id
eb58a1c5-74c4-426c-89bd-a8b1d0a57af6 (old id 109264)
alternative location
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12115614&dopt=Abstract
date added to LUP
2007-07-19 15:21:31
date last changed
2017-06-18 03:35:56
@article{eb58a1c5-74c4-426c-89bd-a8b1d0a57af6,
  abstract     = {We have investigated the role of B cells in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) using B cell-deficient mice muMT) and mice bearing the X-linked immunodeficiency (xid). The mice were immunized with MOG(1-125 )in complete Freund's adjuvant but without use of pertussis toxin. B cell-deficient muMT mice on different genetic backgrounds (C57BL/10 and DBA/1 strains) developed EAE, although with a reduced clinical severity. Histological analyses revealed decreased demyelination in the central nervous system while the influx of inflammatory cells was similar or only slightly reduced as compared to B cell-sufficient control mice. Xid mice on the DBA/1 background also developed disease with a reduced disease severity. The anti-MOG antibody response in the xid mice was decreased, while the T cell response to MOG was unaffected. We thus demonstrate that B cells are not critical for the development of MOG-induced EAE but contribute to the severity. The contribution of B cells to pathogenesis appears to be mainly through demyelination rather than through inflammation.},
  author       = {Svensson, Lars and Abdul-Majid, Khairul-Bariah and Bauer, Jan and Lassmann, Hans and Harris, Robert A and Holmdahl, Rikard},
  issn         = {1521-4141},
  keyword      = {Non-U.S. Gov't,Support,Rats,Myelin-Associated Glycoprotein : adverse effects,Myelin Sheath : metabolism,Inbred DBA,Mice,Inbred C57BL,Male,Immunologic Deficiency Syndromes,Female,Encephalomyelitis,Experimental Autoimmune : pathology,T-Lymphocytes : immunology,Experimental Autoimmune : chemically induced,Demyelinating Diseases,Comparative Study,Central Nervous System : pathology,B-Lymphocytes : immunology,Animal},
  language     = {eng},
  number       = {7},
  pages        = {1939--1946},
  publisher    = {John Wiley & Sons},
  series       = {European Journal of Immunology},
  title        = {A comparative analysis of B cell-mediated myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis pathogenesis in B cell-deficient mice reveals an effect on demyelination.},
  url          = {http://dx.doi.org/10.1002/1521-4141(200207)32:7<1939::AID-IMMU1939>3.0.CO;2-S},
  volume       = {32},
  year         = {2002},
}