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Role of glycopeptide-specific T cells in collagen-induced arthritis: an example how post-translational modification of proteins may be involved in autoimmune disease

Corthay, Alexandre; Bäcklund, Johan LU and Holmdahl, Rikard LU (2001) In Annals of Medicine 33(7). p.456-465
Abstract
Immunization of mice with type II collagen (CII), a cartilage-restricted protein, leads to collagen-induced arthritis (CIA), a model for rheumatoid arthritis (RA). CIA symptoms consist of an erosive joint inflammation caused by an autoimmune attack, mediated by both T and B lymphocytes. CD4+ alphabeta T cells play a central role in CIA, both by helping B cells to produce anti-CII antibodies, and by interacting with other cells in the joints, eg macrophages. In H-2q mice, most CII-specific CD4+ T cells recognize the CII(256-270) peptide presented on the major histocompatibility complex (MHC) class II Aq molecule. Post-translational modifications (hydroxylation and variable glycosylation) of the lysine residue at position 264 of CII generate... (More)
Immunization of mice with type II collagen (CII), a cartilage-restricted protein, leads to collagen-induced arthritis (CIA), a model for rheumatoid arthritis (RA). CIA symptoms consist of an erosive joint inflammation caused by an autoimmune attack, mediated by both T and B lymphocytes. CD4+ alphabeta T cells play a central role in CIA, both by helping B cells to produce anti-CII antibodies, and by interacting with other cells in the joints, eg macrophages. In H-2q mice, most CII-specific CD4+ T cells recognize the CII(256-270) peptide presented on the major histocompatibility complex (MHC) class II Aq molecule. Post-translational modifications (hydroxylation and variable glycosylation) of the lysine residue at position 264 of CII generate at least four different T-cell determinants that are specifically recognized by distinct T-cell subsets. Most T cells recognize CII(256-270) glycosylated with the monosaccharide galactose, which is consequently immunodominant in CIA. Recent studies indicate that the arthritogenic T cells in CIA are glycopeptide-specific, suggesting that induction of self-tolerance may be rendered more difficult by glycosylation of CII. These data open the possibility that outoimmune disease may be caused by the creation of new epitopes by posttranslational modification of proteins under circumstances such as trauma, inflammation or ageing. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
arthritis, autoimmunity, collagen-induced arthritis, glycosylation/glycopeptide, peptide, post-translational modification, T lymphocyte
in
Annals of Medicine
volume
33
issue
7
pages
456 - 465
publisher
Informa Healthcare
external identifiers
  • pmid:11680793
  • scopus:0034786078
ISSN
1365-2060
DOI
10.3109/07853890109002094
language
English
LU publication?
yes
id
95c6fbbb-e865-4e71-be82-4cffab9581ee (old id 1120203)
date added to LUP
2008-06-26 09:23:31
date last changed
2018-05-29 10:57:03
@article{95c6fbbb-e865-4e71-be82-4cffab9581ee,
  abstract     = {Immunization of mice with type II collagen (CII), a cartilage-restricted protein, leads to collagen-induced arthritis (CIA), a model for rheumatoid arthritis (RA). CIA symptoms consist of an erosive joint inflammation caused by an autoimmune attack, mediated by both T and B lymphocytes. CD4+ alphabeta T cells play a central role in CIA, both by helping B cells to produce anti-CII antibodies, and by interacting with other cells in the joints, eg macrophages. In H-2q mice, most CII-specific CD4+ T cells recognize the CII(256-270) peptide presented on the major histocompatibility complex (MHC) class II Aq molecule. Post-translational modifications (hydroxylation and variable glycosylation) of the lysine residue at position 264 of CII generate at least four different T-cell determinants that are specifically recognized by distinct T-cell subsets. Most T cells recognize CII(256-270) glycosylated with the monosaccharide galactose, which is consequently immunodominant in CIA. Recent studies indicate that the arthritogenic T cells in CIA are glycopeptide-specific, suggesting that induction of self-tolerance may be rendered more difficult by glycosylation of CII. These data open the possibility that outoimmune disease may be caused by the creation of new epitopes by posttranslational modification of proteins under circumstances such as trauma, inflammation or ageing.},
  author       = {Corthay, Alexandre and Bäcklund, Johan and Holmdahl, Rikard},
  issn         = {1365-2060},
  keyword      = {arthritis,autoimmunity,collagen-induced arthritis,glycosylation/glycopeptide,peptide,post-translational modification,T lymphocyte},
  language     = {eng},
  number       = {7},
  pages        = {456--465},
  publisher    = {Informa Healthcare},
  series       = {Annals of Medicine},
  title        = {Role of glycopeptide-specific T cells in collagen-induced arthritis: an example how post-translational modification of proteins may be involved in autoimmune disease},
  url          = {http://dx.doi.org/10.3109/07853890109002094},
  volume       = {33},
  year         = {2001},
}