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.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/130902
- author
- Kutty Selva, Nandakumar LU ; Bäcklund, Johan LU ; Vestberg, Mikael LU and Holmdahl, Rikard LU
- organization
- publishing date
- 2004
- 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 (BMC)
- external identifiers
-
- wos:000225160100012
- pmid:15535832
- scopus:17444405097
- pmid:15535832
- ISSN
- 1478-6362
- DOI
- 10.1186/ar1217
- 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
- 2cdf61c7-4963-4f66-973f-0d9932803748 (old id 130902)
- date added to LUP
- 2016-04-01 11:40:42
- date last changed
- 2022-04-12 23:35:26
@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}},
keywords = {{T cells; monoclonal antibodies; collagen type II; arthritis; B cells}},
language = {{eng}},
number = {{6}},
pages = {{544--550}},
publisher = {{BioMed Central (BMC)}},
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 = {{https://lup.lub.lu.se/search/files/2591053/624174.pdf}},
doi = {{10.1186/ar1217}},
volume = {{6}},
year = {{2004}},
}