Glycosylation of type II collagen is of major importance for T cell tolerance and pathology in collagen-induced arthritis.
(2002) In European Journal of Immunology 32(12). p.3776-3784- Abstract
- Type II collagen (CII) is a candidate cartilage-specific autoantigen, which can become post-translationally modified by hydroxylation and glycosylation. T cell recognition of CII is essential for the development of murine collagen-induced arthritis (CIA) and also occurs in rheumatoid arthritis (RA). The common denominator of murine CIA and human RA is the presentation of an immunodominant CII-derived glycosylated peptide on murine Aq and human DR4 molecules, respectively. To investigate the importance of T cell recognition of glycosylated CII in CIA development after immunization with heterologous CII, we treated neonatal mice with different heterologous CII-peptides (non-modified, hydroxylated and galactosylated). Treatment with the... (More)
- Type II collagen (CII) is a candidate cartilage-specific autoantigen, which can become post-translationally modified by hydroxylation and glycosylation. T cell recognition of CII is essential for the development of murine collagen-induced arthritis (CIA) and also occurs in rheumatoid arthritis (RA). The common denominator of murine CIA and human RA is the presentation of an immunodominant CII-derived glycosylated peptide on murine Aq and human DR4 molecules, respectively. To investigate the importance of T cell recognition of glycosylated CII in CIA development after immunization with heterologous CII, we treated neonatal mice with different heterologous CII-peptides (non-modified, hydroxylated and galactosylated). Treatment with the galactosylated peptide (galactoseat position 264) was superior in protecting mice from CIA. Protection was accompanied by a reduced antibody response to CII and by an impaired T cell response to the glycopeptide. To investigate the importance of glycopeptide recognition in an autologous CIA model, we treated MMC-transgenic mice, which express the heterologous CII epitope with a glutamic acid in position 266 in cartilage, with CII-peptides. Again, a strong vaccination potential of the glycopeptide was seen. Hence CII-glycopeptides may be the optimal choice of vaccination target in RA, since humans share the same epitope as the MMC mouse (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/112927
- author
- Bäcklund, Johan LU ; Treschow, Alexandra LU ; Bockermann, Robert LU ; Holm, Björn ; Holm, Lotta ; Issazadeh-Navikas, Shohreh ; Kihlberg, Jan and Holmdahl, Rikard LU
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Mice, Male, Immune Tolerance, Human, Glycosylation, Female, Inbred C3H, Non-U.S. Gov't, T-Lymphocytes: immunology, Transgenic, Collagen Type II: genetics, Collagen Type II: chemistry, Autoimmunity, Rheumatoid: immunology, Support, Cross Reactions, Collagen Type II: immunology, Arthritis, Animal, Experimental: immunology, Experimental: metabolism, Experimental: pathology, Rheumatoid: etiology
- in
- European Journal of Immunology
- volume
- 32
- issue
- 12
- pages
- 3776 - 3784
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000179907000047
- scopus:0036919338
- ISSN
- 1521-4141
- DOI
- 10.1002/1521-4141(200212)32:12<3776::AID-IMMU3776>3.0.CO;2-A
- 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
- 7b664def-176d-460a-80d8-3436174306b9 (old id 112927)
- date added to LUP
- 2016-04-01 12:16:34
- date last changed
- 2022-01-27 01:23:01
@article{7b664def-176d-460a-80d8-3436174306b9,
abstract = {{Type II collagen (CII) is a candidate cartilage-specific autoantigen, which can become post-translationally modified by hydroxylation and glycosylation. T cell recognition of CII is essential for the development of murine collagen-induced arthritis (CIA) and also occurs in rheumatoid arthritis (RA). The common denominator of murine CIA and human RA is the presentation of an immunodominant CII-derived glycosylated peptide on murine Aq and human DR4 molecules, respectively. To investigate the importance of T cell recognition of glycosylated CII in CIA development after immunization with heterologous CII, we treated neonatal mice with different heterologous CII-peptides (non-modified, hydroxylated and galactosylated). Treatment with the galactosylated peptide (galactoseat position 264) was superior in protecting mice from CIA. Protection was accompanied by a reduced antibody response to CII and by an impaired T cell response to the glycopeptide. To investigate the importance of glycopeptide recognition in an autologous CIA model, we treated MMC-transgenic mice, which express the heterologous CII epitope with a glutamic acid in position 266 in cartilage, with CII-peptides. Again, a strong vaccination potential of the glycopeptide was seen. Hence CII-glycopeptides may be the optimal choice of vaccination target in RA, since humans share the same epitope as the MMC mouse}},
author = {{Bäcklund, Johan and Treschow, Alexandra and Bockermann, Robert and Holm, Björn and Holm, Lotta and Issazadeh-Navikas, Shohreh and Kihlberg, Jan and Holmdahl, Rikard}},
issn = {{1521-4141}},
keywords = {{Mice; Male; Immune Tolerance; Human; Glycosylation; Female; Inbred C3H; Non-U.S. Gov't; T-Lymphocytes: immunology; Transgenic; Collagen Type II: genetics; Collagen Type II: chemistry; Autoimmunity; Rheumatoid: immunology; Support; Cross Reactions; Collagen Type II: immunology; Arthritis; Animal; Experimental: immunology; Experimental: metabolism; Experimental: pathology; Rheumatoid: etiology}},
language = {{eng}},
number = {{12}},
pages = {{3776--3784}},
publisher = {{John Wiley & Sons Inc.}},
series = {{European Journal of Immunology}},
title = {{Glycosylation of type II collagen is of major importance for T cell tolerance and pathology in collagen-induced arthritis.}},
url = {{http://dx.doi.org/10.1002/1521-4141(200212)32:12<3776::AID-IMMU3776>3.0.CO;2-A}},
doi = {{10.1002/1521-4141(200212)32:12<3776::AID-IMMU3776>3.0.CO;2-A}},
volume = {{32}},
year = {{2002}},
}