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对恶唑酮在体内刺激的淋巴结细胞的糖皮质激素敏感性。

Sensitivity to glucocorticoids of lymph node cells stimulated in vivo by oxazolone.

作者信息

Venetianer A, Arányi P, Bösze Z S, Fachet J

出版信息

Scand J Immunol. 1978;8(4):355-62. doi: 10.1111/j.1365-3083.1978.tb00529.x.

Abstract

Sensitization of B10.A mice with oxazolone results in delayed-type hypersensitivity (DTH) and a two to three-fold increase in the weight of regional lymph nodes by the third day. Hydrocortisone treatment of the animals 3 days after sensitization suppresses the manifestation of DTH on the tenth day but not on the seventieth day and significantly decreases the weight of lymph nodes both in control and oxazolone-sensitized mice. The regional lymph node cells of oxazolone-stimulated mice were, like the controls, sensitive to dexamethasone in vitro, as judged by viability and thymidine incorporation. Dexamethasone binding capacity of the regional lymph node cells 72 h after oxazolone sensitization increased. However, the dissociation constant for dexamethasone, the binding specificity, and the nuclear transfer of the hormone were not altered. Since high doses of hydrocortisone given 3 days after sensitization were unable to erase permanently the DTH to oxazolone, it seems very likely that cells responsible for the immunological memory survive the high dose of hydrocortisone.

摘要

用恶唑酮致敏B10.A小鼠会导致迟发型超敏反应(DTH),到第三天时局部淋巴结重量增加两到三倍。致敏3天后对动物进行氢化可的松治疗可抑制第十天DTH的表现,但不能抑制第七十天的表现,且显著降低对照组和恶唑酮致敏小鼠的淋巴结重量。通过活力和胸腺嘧啶核苷掺入判断,恶唑酮刺激小鼠的局部淋巴结细胞与对照组一样,在体外对地塞米松敏感。恶唑酮致敏72小时后局部淋巴结细胞的地塞米松结合能力增强。然而,地塞米松的解离常数、结合特异性和激素的核转运未改变。由于致敏3天后给予高剂量氢化可的松无法永久消除对恶唑酮的DTH,很可能负责免疫记忆的细胞在高剂量氢化可的松治疗后存活下来。

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