Hutchings P R, Cooke A, Dawe K, Champion B R, Geysen M, Valerio R, Roitt I M
Immunology Department, University College and Middlesex Medical School, London, United Kingdom.
J Exp Med. 1992 Mar 1;175(3):869-72. doi: 10.1084/jem.175.3.869.
A synthetic peptide based on a sequence containing thyroxine at position 2553 in thyroglobulin (Tg), and already shown to be recognized by two clonotypically distinct murine Tg autoreactive T cell hybridomas, can trigger primed lymph node cells to transfer thyroiditis to naive recipients. Donor lymph node cells could be prepared from mice immunized either with intact mouse Tg or with this peptide itself. After a second exposure to the priming antigen in vitro, both these populations induced 100% thyroiditis in recipient animals. The importance of the T4 residue in the development of disease was demonstrated by the failure of Tg tryptic peptides depleted of T4 to stimulate pathogenic effectors in vitro, even when the lymph node cells had been taken from mice primed with whole Tg. We conclude that this T4-containing 12mer sequence is a major thyroiditogenic epitope in CBA/J mice although we cannot exclude the possibility that there are other pathogenic epitopes present in the whole Tg molecule.
一种基于甲状腺球蛋白(Tg)第2553位含甲状腺素序列的合成肽,已被证明可被两种克隆型不同的鼠源Tg自身反应性T细胞杂交瘤识别,它能触发致敏淋巴结细胞将甲状腺炎转移至未致敏受体。供体淋巴结细胞可从小鼠制备,这些小鼠要么用完整的小鼠Tg免疫,要么用该肽本身免疫。在体外再次接触致敏抗原后,这两种细胞群体均在受体动物中诱发了100%的甲状腺炎。Tg胰蛋白酶肽段去除T4后无法在体外刺激致病效应细胞,即使淋巴结细胞取自用全Tg致敏的小鼠,这证明了T4残基在疾病发展中的重要性。我们得出结论,这个含T4的12聚体序列是CBA/J小鼠中的主要致甲状腺炎表位,尽管我们不能排除整个Tg分子中存在其他致病表位的可能性。