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T-2毒素的局部应用可抑制BALB/c小鼠的接触性超敏反应。

Topical application of T-2 toxin inhibits the contact hypersensitivity response in BALB/c mice.

作者信息

Blaylock B L, Kouchi Y, Comment C E, Pollock P L, Luster M I

机构信息

Environmental Immunology Section, National Institute of Environmental Health Sciences/NIH, Research Triangle Park, NC 27709.

出版信息

J Immunol. 1993 Jun 1;150(11):5135-43.

PMID:8496607
Abstract

T-2 toxin, a trichothecene mycotoxin, has previously been shown to alter immune functions and promote skin tumors. We demonstrate that topically applied T-2 toxin reduces the ear swelling response to oxazolone challenge in BALB/c mice. For this reduction in ear swelling to occur, toxin application must be at, or within, 1 h after challenge. Dose-response studies showed a 44% reduction in ear swelling with 30 ng of T-2 toxin as compared with a similar reduction with 300 ng of dexamethasone. T-2 toxin did not affect Ag transport from the challenge site to the draining lymph nodes as measured by FITC transport. However, T-2 toxin significantly reduced both MHC class II (Ia) expression and Ag presentation at the same concentrations. Because T-2 toxin, a known protein synthesis inhibitor, was found to inhibit protein synthesis in epidermal cell cultures as measured by [3H]-leucine incorporation, cycloheximide was also examined. Cycloheximide reduced both oxazolone-induced ear swelling and Ag presentation in a similar manner to T-2 toxin. One mechanism of action for T-2 toxin in reducing the contact hypersensitivity response is via inhibition of protein synthesis and effective Ag presentation by epidermal Langerhans cells. This may involve alterations in Ia Ag expression, although a role for class II in the induction phase of the contact hypersensitivity response has not been established definitively.

摘要

T-2毒素是一种单端孢霉烯族霉菌毒素,先前已被证明可改变免疫功能并促进皮肤肿瘤的发生。我们证明,局部应用T-2毒素可降低BALB/c小鼠对恶唑酮攻击的耳部肿胀反应。为了出现这种耳部肿胀的减轻,毒素必须在攻击后1小时内或1小时时应用。剂量反应研究表明,与300 ng地塞米松产生的类似减轻效果相比,30 ng T-2毒素可使耳部肿胀减轻44%。通过FITC转运测量发现,T-2毒素不影响抗原从攻击部位向引流淋巴结的转运。然而,在相同浓度下,T-2毒素显著降低了MHC II类(Ia)表达和抗原呈递。由于T-2毒素是一种已知的蛋白质合成抑制剂,通过[3H]-亮氨酸掺入法测量发现它可抑制表皮细胞培养物中的蛋白质合成,因此也对放线菌酮进行了检测。放线菌酮以与T-2毒素类似的方式降低了恶唑酮诱导的耳部肿胀和抗原呈递。T-2毒素降低接触性超敏反应的一种作用机制是通过抑制蛋白质合成以及表皮朗格汉斯细胞有效的抗原呈递。这可能涉及Ia抗原表达的改变,尽管II类在接触性超敏反应诱导阶段的作用尚未明确确立。

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