Myers L K, Seyer J M, Stuart J M, Terato K, David C S, Kang A H
Department of Pediatrics, University of Tennessee, Memphis 38163.
J Immunol. 1993 Jul 1;151(1):500-5.
Chick type II collagen (CII), a protein commonly found in joint cartilage, induces an autoimmune arthritis when administered to susceptible strains of mice. A cyanogen bromide fragment of CII, CB11, contains the requisite epitopes critical for inducing collagen-induced arthritis. If administered as a tolerogen, however, before immunization, CB11 prevents the onset of disease. Therefore, delineation of structural elements of CB11 that can regulate autoreactive T cells became the goal of this study. To delineate the structural elements of CB11 antigenic to T cells, 14 peptides containing overlapping sequences of CB11 were generated. Mononuclear cells from CII-immunized DBA/1 mice were cultured with these peptides and the resulting supernatants examined for the production of IFN-gamma. Two peptides, CII 181-209 and CII 245-270, generated the greatest responses. The ability of these two peptides to regulate arthritis was tested by administering them to neonatal DBA/1 mice as tolerogens before immunization with CII. Both peptides suppressed the incidence of arthritis whereas no other peptide used as a tolerogen significantly altered the course of the disease. T cells from four arthritis-resistant murine strains did not recognize either peptide when immunized with CII, whereas cells from the disease-susceptible B10.Q mice responded well to both. Thus, the coincidence of T cell responses to CII 181-209 and CII 245-270 in CIA-susceptible mice and the lack of response in disease-resistant strains or CII-tolerized mice identify these two peptides as containing important T cell epitopes that regulate CIA.
鸡II型胶原蛋白(CII)是一种常见于关节软骨中的蛋白质,当将其注射到易患该疾病的小鼠品系中时,会引发自身免疫性关节炎。CII的溴化氰片段CB11包含诱导胶原诱导性关节炎所需的关键表位。然而,如果在免疫前将CB11作为耐受原给药,则可预防疾病的发生。因此,确定CB11中能够调节自身反应性T细胞的结构元件成为本研究的目标。为了确定CB11对T细胞具有抗原性的结构元件,制备了14个包含CB11重叠序列的肽段。用这些肽段培养来自经CII免疫的DBA/1小鼠的单核细胞,并检测所得上清液中干扰素-γ的产生。两个肽段CII 181-209和CII 245-270产生了最强的反应。通过在新生DBA/1小鼠免疫CII前将这两个肽段作为耐受原给药,来测试它们调节关节炎的能力。这两个肽段均抑制了关节炎的发病率,而用作耐受原的其他肽段均未显著改变疾病进程。用CII免疫时,来自四种抗关节炎小鼠品系的T细胞均不识别这两个肽段,而来自疾病易感的B10.Q小鼠的细胞对这两个肽段均有良好反应。因此,在胶原诱导性关节炎易感小鼠中T细胞对CII 181-209和CII 245-270的反应与在抗病品系或经CII耐受的小鼠中缺乏反应的情况表明,这两个肽段包含调节胶原诱导性关节炎的重要T细胞表位。