## Abstract ## Objective Previous studies have shown that an analog peptide of the immunodominant T cell determinant of type II collagen (CII), i.e., CII^256β276^(N^263^, D^266^), was able to suppress the immune response to CII and the development of arthritis in DR1βtransgenic mice. The present s
Juvenile arthritis and autoimmunity to type II collagen
β Scribed by L. K. Myers; G. C. Higgins; T. H. Finkel; A. M. Reed; J. W. Thompson; R. C. Walton; J. Hendrickson; N. C. Kerr; R. K. Pandya-Lipman; B. V. Shlopov; P. Stastny; A. E. Postlethwaite; A. H. Kang
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 79 KB
- Volume
- 44
- Category
- Article
- ISSN
- 0004-3591
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β¦ Synopsis
Objective. Joint inflammation in juvenile rheumatoid arthritis (JRA) is sometimes associated with an autoimmune response to type II collagen (CII), a cartilage-specific protein. To test the hypothesis that down-regulation of autoimmunity to CII can be accomplished in JRA by oral administration of CII, an openlabel study of CII was performed in 9 patients with JRA.
Methods. Seven rheumatoid factor-negative JRA patients with polyarticular disease and 2 JRA patients with pauciarticular disease (1 with early onset and 1 with late onset) were treated for 3 months with oral bovine CII. Patients were examined for disease activity and underwent routine laboratory testing at monthly intervals. Two of the patients had flares of disease when treatment was discontinued, and these patients were re-treated for an additional 3 months. To test the hypothesis that oral tolerance induces an immune deviation of T cells, peripheral blood mononuclear cells from patients were collected before and after treatment and cultured with CII. Supernatants and RNA were collected and analyzed for the presence of various cytokines.
Results. Eight patient trials met the criteria for
π SIMILAR VOLUMES
## Abstract ## Objective To establish a new animal model in DRB1\*0401 (DR4)βtransgenic mice in which T cell tolerance to self type II collagen (CII) can be broken and allow for the development of autoimmune arthritis, to investigate the role of posttranslational modifications of the CII^259β273^