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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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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
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 Inc.
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
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)
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
2016-04-01 11:53:39
date last changed
2022-04-05 06:39:28
@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}},
  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}},
  language     = {{eng}},
  number       = {{7}},
  pages        = {{1939--1946}},
  publisher    = {{John Wiley & Sons Inc.}},
  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}},
  doi          = {{10.1002/1521-4141(200207)32:7<1939::AID-IMMU1939>3.0.CO;2-S}},
  volume       = {{32}},
  year         = {{2002}},
}