Ohnishi Yasuyuki, Tsutsumi Akito, Matsumoto Isao, Goto Daisuke, Ito Satoshi, Kuwana Masataka, Uemura Yasushi, Nishimura Yasuharu, Sumida Takayuki
Division of Rheumatology, Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tenodai, Tsukuba, 305-8575, Japan.
Mod Rheumatol. 2006;16(4):226-8. doi: 10.1007/s10165-006-0495-1.
We previously reported that peripheral blood mononuclear cells from HLA-DRB10101 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-DRB10101 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.
我们之前报道过,来自 HLA - DRB10101 的日本类风湿关节炎(RA)患者的外周血单核细胞对 II 型胶原(CII)的 256 - 271 肽具有高度反应性。在本报告中,我们试图通过改变肽配体(APL)来调节 HLA - DRB10101 的 RA 患者 T 细胞对 CII 的反应性,APL 是 CII 256 - 271 肽上 T 细胞表位的单个氨基酸替换。使用三种不同的 T 细胞系评估了 21 种 APL 的拮抗活性。结果显示,CII 256 - 271 的 262(G→A)APL 在所有 T 细胞系中均表现出拮抗活性,提示应用 CII APL 可能是调节 RA 的一种新治疗策略。