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格雷夫斯病患者的辅助性T细胞亚群对自身甲状腺细胞和甲状腺内T细胞产生显著增殖反应。

The remarkable proliferation of helper T cell subset in response to autologous thyrocytes and intrathyroidal T cells from patients with Graves' disease.

作者信息

Eguchi K, Otsubo T, Kawabe Y, Ueki Y, Fukuda T, Matsunaga M, Shimomura C, Ishikawa N, Tezuka H, Nakao H

机构信息

First Department of Internal Medicine, Nagasaki University School of Medicine.

出版信息

Clin Exp Immunol. 1987 Nov;70(2):403-10.

Abstract

We have studied cellular interactions among thyrocytes, intrathyroidal T cells and peripheral blood T cells from Graves' patients. In the autologous mixed lymphocyte reaction of Graves' patients, CD4+ cells were able to proliferate vigorously against autologous non-T cells, whereas CD8+ cells responded weakly to non-T cell stimulators. Furthermore, the proliferative response of the CD4+ 2H4+ suppressor-inducer T cell subset was increased like that of the CD4+ 2H4- helper T cell subset. In contrast to peripheral blood non-T cell stimulators, thyrocytes and intrathyroidal T cells had the ability to activate the CD4+ 2H4- helper T cell subset but were not able to cause proliferation both of CD4+ 2H4+ suppressor-inducer T cell and CD8+ suppressor/cytotoxic T cell subsets. The marked reduction in proliferative responses of CD4+ 2H4+ cells and CD8+ cells could not be attributed to a difference in kinetics or altered response to variable number of stimulator cells. On the basis of these findings, it is suggested that the concentration of the helper T cell subset may be progressively increased and suppressor circuits may be unable to be activated in thyroid tissues. These abnormalities in cellular interactions may induce the excessive production of autoantibodies.

摘要

我们研究了格雷夫斯病患者甲状腺细胞、甲状腺内T细胞和外周血T细胞之间的细胞相互作用。在格雷夫斯病患者的自体混合淋巴细胞反应中,CD4+细胞能够针对自体非T细胞强烈增殖,而CD8+细胞对非T细胞刺激物反应较弱。此外,CD4+ 2H4+抑制诱导性T细胞亚群的增殖反应与CD4+ 2H4-辅助性T细胞亚群一样增加。与外周血非T细胞刺激物不同,甲状腺细胞和甲状腺内T细胞能够激活CD4+ 2H4-辅助性T细胞亚群,但不能引起CD4+ 2H4+抑制诱导性T细胞亚群和CD8+抑制/细胞毒性T细胞亚群的增殖。CD4+ 2H4+细胞和CD8+细胞增殖反应的显著降低不能归因于动力学差异或对不同数量刺激细胞反应的改变。基于这些发现提示,甲状腺组织中辅助性T细胞亚群的浓度可能逐渐增加,抑制回路可能无法被激活。这些细胞相互作用的异常可能导致自身抗体的过度产生。

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