ORIGINAL ARTICLE
Altered peptide ligands control type II collagen-reactive T cells from rheumatoid arthritis patients
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Yasuyuki Ohnish1, Akito Tsutsumi1, Isao Matsumoto1, Daisuke Goto1,
Satoshi Ito1, Masataka Kuwana2, Yasushi Uemura3, Yasuharu Nishimura4
and Takayuki Sumida1
| (1) |
Division of Rheumatology, Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tenodai, Tsukuba 305-8575, Japan |
| (2) |
Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan |
| (3) |
Department of Allergy and Immunology, Saitama Medical University, Moroyama, Saitama, Japan |
| (4) |
IDepartment of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan |
Received: 04 April 2006 Accepted: 22 May 2006
Abstract We previously reported that peripheral blood mononuclear cells from HLA-DRB1*0101 Japanese patients with rheumatoid arthritis (RA) were highly reactive to 256?271 peptide of type II collagen (CII). In this report, we tried to regulate the CII reactivity of T cells from RA patients with HLA-DRB1*0101 by altered peptide ligand (APL), which is a single amino acid substitution of the T-cell epitope on CII 256?271 peptide. Antagonistic activity of 21 APLs was assessed using three different T-cell lines. Results showed that 262 (G→A) APL of CII 256?271 exhibited antagonistic activity in all T-cell lines and it was suggested that the application of CII APL might be a new therapeutic strategy in the regulation of RA.
Key words Altered peptide ligand (APL) - Antagonist - Rheumatoid arthritis (RA) - T cells - Type II collagen
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