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Collagen type II (CII)-specific antibodies induce arthritis in the absence of T or B cells but the arthritis progression is enhanced by CII-reactive T cells.

Kutty Selva, Nandakumar LU ; Bäcklund, Johan LU ; Vestberg, Mikael LU and Holmdahl, Rikard LU (2004) In Arthritis Research and Therapy 6(6). p.544-550
Abstract
Antibodies against type II collagen (anti-CII) are arthritogenic and have a crucial role in the initiation of collagen-induced arthritis. Here, we have determined the dependence of T and B cells in collagen-antibody-induced arthritis (CAIA) during different phases of arthritis. Mice deficient for B and/or T cells were susceptible to the CAIA, showing that the antibodies induce arthritis even in the absence of an adaptive immune system. To determine whether CII-reactive T cells could have a role in enhancing arthritis development at the effector level of arthritis pathogenesis, we established a T cell line reactive with CII. This T cell line was oligoclonal and responded to different post-translational forms of the major CII epitope at... (More)
Antibodies against type II collagen (anti-CII) are arthritogenic and have a crucial role in the initiation of collagen-induced arthritis. Here, we have determined the dependence of T and B cells in collagen-antibody-induced arthritis (CAIA) during different phases of arthritis. Mice deficient for B and/or T cells were susceptible to the CAIA, showing that the antibodies induce arthritis even in the absence of an adaptive immune system. To determine whether CII-reactive T cells could have a role in enhancing arthritis development at the effector level of arthritis pathogenesis, we established a T cell line reactive with CII. This T cell line was oligoclonal and responded to different post-translational forms of the major CII epitope at position 260–270 bound to the Aq class II molecule. Importantly, it cross-reacted with the mouse peptide although it is bound with lower affinity to the Aq molecule than the corresponding rat peptide. The T cell line could not induce clinical arthritis per se in Aq-expressing mice even if these mice expressed the major heterologous CII epitope in cartilage, as in the transgenic MMC (mutated mouse collagen) mouse. However, a combined treatment with anti-CII monoclonal antibodies and CII-reactive T cells enhanced the progression of severe arthritis. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
T cells, monoclonal antibodies, collagen type II, arthritis, B cells
in
Arthritis Research and Therapy
volume
6
issue
6
pages
544 - 550
publisher
BioMed Central
external identifiers
  • wos:000225160100012
  • pmid:15535832
  • scopus:17444405097
ISSN
1478-6362
DOI
10.1186/ar1217
language
English
LU publication?
yes
id
2cdf61c7-4963-4f66-973f-0d9932803748 (old id 130902)
date added to LUP
2007-07-16 13:24:05
date last changed
2017-10-29 03:26:16
@article{2cdf61c7-4963-4f66-973f-0d9932803748,
  abstract     = {Antibodies against type II collagen (anti-CII) are arthritogenic and have a crucial role in the initiation of collagen-induced arthritis. Here, we have determined the dependence of T and B cells in collagen-antibody-induced arthritis (CAIA) during different phases of arthritis. Mice deficient for B and/or T cells were susceptible to the CAIA, showing that the antibodies induce arthritis even in the absence of an adaptive immune system. To determine whether CII-reactive T cells could have a role in enhancing arthritis development at the effector level of arthritis pathogenesis, we established a T cell line reactive with CII. This T cell line was oligoclonal and responded to different post-translational forms of the major CII epitope at position 260–270 bound to the Aq class II molecule. Importantly, it cross-reacted with the mouse peptide although it is bound with lower affinity to the Aq molecule than the corresponding rat peptide. The T cell line could not induce clinical arthritis per se in Aq-expressing mice even if these mice expressed the major heterologous CII epitope in cartilage, as in the transgenic MMC (mutated mouse collagen) mouse. However, a combined treatment with anti-CII monoclonal antibodies and CII-reactive T cells enhanced the progression of severe arthritis.},
  author       = {Kutty Selva, Nandakumar and Bäcklund, Johan and Vestberg, Mikael and Holmdahl, Rikard},
  issn         = {1478-6362},
  keyword      = {T cells,monoclonal antibodies,collagen type II,arthritis,B cells},
  language     = {eng},
  number       = {6},
  pages        = {544--550},
  publisher    = {BioMed Central},
  series       = {Arthritis Research and Therapy},
  title        = {Collagen type II (CII)-specific antibodies induce arthritis in the absence of T or B cells but the arthritis progression is enhanced by CII-reactive T cells.},
  url          = {http://dx.doi.org/10.1186/ar1217},
  volume       = {6},
  year         = {2004},
}