Weetman A P
Department of Medicine, University of Cambridge Clinical School, Addenbrooke's Hospital, United Kingdom.
Clin Immunol Immunopathol. 1989 May;51(2):303-10. doi: 10.1016/0090-1229(89)90028-7.
To assess whether there is a defect in thyroid antigen-specific suppressor cells in Hashimoto's thyroiditis (HT) and whether such cells actively prevent thyroid autoreactivity in control subjects, T cell proliferation was measured before and after removal of CD8-positive cells from the lymphocyte population. CD8 depletion significantly increased the proliferation of HT lymphocytes to soluble thyroglobulin and to thyroid microsomal antigen immunoblotted onto nitrocellulose; some of these cultures also reacted with an unidentified thyroid antigen, mol wt approx 16 kDa. However, CD8 depletion did not permit normal lymphocytes to respond to thyroid antigens. Peripheral blood CD8 cells were also found to suppress proliferation of a thyroid T cell line, derived from a patient with HT, in response to autologous, Ia-positive thyroid follicular cells. These results do not support the existence of a defect in antigen-specific suppressor cells in HT, nor the active suppression of thyroid autoreactivity by such cells in normal subjects. The data suggest that there may be an imbalance in T cell helper and suppressor influences in thyroiditis, but in some patients a new balance is achieved, so that T cell sensitization to thyroid autoantigens can only be identified by removal of CD8-positive cells.
为了评估桥本甲状腺炎（HT）患者甲状腺抗原特异性抑制细胞是否存在缺陷，以及这些细胞在对照受试者中是否能有效抑制甲状腺自身反应性，在从淋巴细胞群体中去除CD8阳性细胞之前和之后测量了T细胞增殖。去除CD8显著增加了HT淋巴细胞对可溶性甲状腺球蛋白以及印迹在硝酸纤维素膜上的甲状腺微粒体抗原的增殖反应；其中一些培养物还与一种分子量约为16 kDa的未鉴定甲状腺抗原发生反应。然而，去除CD8并不能使正常淋巴细胞对甲状腺抗原产生反应。还发现外周血CD8细胞可抑制源自HT患者的甲状腺T细胞系对自体Ia阳性甲状腺滤泡细胞的增殖反应。这些结果不支持HT患者存在抗原特异性抑制细胞缺陷，也不支持正常受试者中此类细胞对甲状腺自身反应性的有效抑制。数据表明，甲状腺炎中T细胞辅助和抑制作用可能存在失衡，但在一些患者中会达到新的平衡，因此只有通过去除CD8阳性细胞才能识别出T细胞对甲状腺自身抗原的致敏。
