趋化因子通过吸引自身反应性或调节性T细胞来调节实验性自身免疫性甲状腺炎。

Chemokines modulate experimental autoimmune thyroiditis through attraction of autoreactive or regulatory T cells.

作者信息

Goulvestre Claire, Batteux Frédéric, Charreire Jeannine

机构信息

Laboratoire d'Immunologie, Hôpital et Faculté de Médecine Cochin, AP-HP, Université Paris V, Paris, France.

出版信息

Eur J Immunol. 2002 Dec;32(12):3435-42. doi: 10.1002/1521-4141(200212)32:12<3435::AID-IMMU3435>3.0.CO;2-5.

DOI:10.1002/1521-4141(200212)32:12<3435::AID-IMMU3435>3.0.CO;2-5

PMID:12432574

Abstract

A critical event in the pathogenesis of experimental autoimmune thyroiditis (EAT) is the entry of thyroid-specific T lymphocytes into the thyroid gland. To investigate the role of soluble mediators in that infiltration, we have assayed the expression of various chemokines in diseased thyroid glands and in cytokine-treated cultures of normal thyroid epithelial cells. MCP-1 (monocyte chemotactic protein-1) and RANTES are produced during EAT and induced in vitro by IFN-gamma, IL-10, TNF-alpha, and IL-1beta. In vitro chemotaxis experiments using immune lymph node (LN) cells showed that RANTES attracted mTg-specific responder LN cells, whereas MCP-1 attracted mTg-specific CD4(+), CD25(+) regulator cells that secreted IL-10. The in vivo transfer of LN T cells attracted in vitro either by RANTES or by MCP-1 confirmed their opposite effects on the course of EAT.

摘要

实验性自身免疫性甲状腺炎（EAT）发病机制中的一个关键事件是甲状腺特异性T淋巴细胞进入甲状腺。为了研究可溶性介质在这种浸润中的作用，我们检测了患病甲状腺组织以及正常甲状腺上皮细胞经细胞因子处理后的培养物中各种趋化因子的表达。EAT期间会产生单核细胞趋化蛋白-1（MCP-1）和调节激活正常T细胞表达和分泌的因子（RANTES），并且在体外可被γ干扰素、白细胞介素-10、肿瘤坏死因子-α和白细胞介素-1β诱导产生。使用免疫淋巴结（LN）细胞进行的体外趋化实验表明，RANTES吸引甲状腺球蛋白特异性应答性LN细胞，而MCP-1吸引分泌白细胞介素-10的甲状腺球蛋白特异性CD4(+)、CD25(+)调节细胞。RANTES或MCP-1在体外吸引的LN T细胞的体内转移证实了它们对EAT病程具有相反的作用。