A comparative analysis of B cell-mediated myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis pathogenesis in B cell-deficient mice reveals an effect on demyelination.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/109264
- author
- Svensson, Lars LU ; Abdul-Majid, Khairul-Bariah ; Bauer, Jan ; Lassmann, Hans ; Harris, Robert A and Holmdahl, Rikard LU
- organization
- publishing date
- 2002
- 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}},
}