Antigen presentation of Type II collagen in rats

Collagen‐induced arthritis (CIA) is a T‐cell dependent disease of rats which follows immunization with bovine type II collagen (bCII). Susceptibility to CIA is linked to the genes encoding the major histocompatibility complex (MHC), suggesting that antigen presentation is important in disease pathog...

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Bibliographic Details
Published in:Clinical and experimental immunology 2001-09, Vol.125 (3), p.478-484
Main Authors: Catchpole, B., Staines, N. A., Hamblin, A. S.
Format: Article
Language:English
Subjects:
Animals
Antigen Presentation
Arthritis - chemically induced
Arthritis - immunology
B cell
B-Lymphocytes - immunology
Biological and medical sciences
CD4 antigen
Collagen - immunology
collagen‐induced arthritis
dendritic cell
Dendritic Cells - immunology
Diseases of the osteoarticular system
Inflammatory joint diseases
Macrophages - immunology
Male
Medical sciences
Original
Rats
Rats, Inbred Strains
T-Lymphocytes - immunology
type II collagen
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Summary:Collagen‐induced arthritis (CIA) is a T‐cell dependent disease of rats which follows immunization with bovine type II collagen (bCII). Susceptibility to CIA is linked to the genes encoding the major histocompatibility complex (MHC), suggesting that antigen presentation is important in disease pathogenesis. Antigen‐presenting cells (APC) (macrophages, dendritic cells (DC) and B cells) were prepared from WA/KIR/KCL rats and presentation of antigen, in the form of native protein (bCII) or synthetic peptide (bCII:184–198), was assessed in T‐cell proliferation assays. Whilst macrophages inhibited proliferative responses to bCII, splenic or thymic low density cells, enriched for DC, presented both bCII and bCII(184–198) peptide. However, bone marrow‐derived DC, which stimulated T‐cell responses to OVA, failed to present bCII, suggesting differences in processing of these two antigens. B‐cell depletion from lymph node cells abrogated the proliferative response to bCII and reconstitution of a T‐cell population with B cells restored the proliferative response, indicating that B cells are important for stimulating T‐cell responses to bCII. B cells play a critical role in CIA by producing pathogenic anti‐bCII antibodies, and we propose that B cells are also important APC which present bCII to CD4+ T cells.
ISSN:0009-9104
1365-2249
DOI:10.1046/j.1365-2249.2001.01618.x