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1-氯-2,4-二硝基苯诱导的迟发型超敏反应诱导期小鼠口腔黏膜中的朗格汉斯细胞

Langerhans' cells in the murine oral mucosa in the inductive phase of delayed type hypersensitivity with 1-chloro-2, 4-dinitrobenzene.

作者信息

Okamura T, Morimoto M, Yamane G, Takahashi S

机构信息

Department of Oral Medicine, Tokyo Dental College, Chiba, Japan.

出版信息

Clin Exp Immunol. 2003 Nov;134(2):188-94. doi: 10.1046/j.1365-2249.2003.02277.x.

Abstract

We created a murine model of delayed-type hypersensitivity (DTH) to 1-chloro-2, 4-dinitrobenzene (DNCB). Using this murine model, we compared oral mucosal sensitization and skin sensitization for the difference in reaction during the elicitation phase. Evaluation of sensitizability, using the mouse ear swelling test (MEST) after oral mucosal or skin sensitization, showed that the ear swelling response peaked 24 h after challenge. The optimal induction concentration was 1.0% in both oral mucosal and skin sensitization, resulting in a positive reaction rate of 100%. However, the ear swelling response 24 h after challenge with the optimal concentration of DNCB (1.0%) was significantly lower in oral mucosal than in skin sensitization. We compared the oral mucosal and skin sensitization sites for the number of Langerhans' cells (LC) and the antigen-presenting capability in the induction phase. The numbers of F4/80+ major histocompatibility complex (MHC) class II+ LC before induction did not differ significantly between the oral mucosa and the skin. After induction, F4/80+ MHC class II+ LC increased in number, but the increase was significantly smaller in the oral mucosa than in the skin. MEST on anti-CD86 antibody-administered mice showed that ear swelling was similarly suppressed after oral mucosal or skin sensitization. In murine models of DTH after oral mucosal sensitization, the number of F4/80+CD86+ LC increased after induction, but the increase was significantly smaller than that in murine models of DTH after skin sensitization. This study showed that, in murine models of DTH, oral mucosal sensitization elicited a weaker reaction than skin sensitization. This was presumably because oral mucosal sensitization induced fewer LC, resulting in lower antigen-presenting capability.

摘要

我们建立了对1-氯-2,4-二硝基苯(DNCB)的迟发型超敏反应(DTH)小鼠模型。利用该小鼠模型,我们比较了口服黏膜致敏和皮肤致敏在激发阶段反应的差异。通过口服黏膜或皮肤致敏后使用小鼠耳肿胀试验(MEST)评估致敏性,结果显示激发后24小时耳肿胀反应达到峰值。口服黏膜致敏和皮肤致敏的最佳诱导浓度均为1.0%,阳性反应率均为100%。然而,用最佳浓度的DNCB(1.0%)激发后24小时,口服黏膜致敏的耳肿胀反应明显低于皮肤致敏。我们比较了口服黏膜和皮肤致敏部位在诱导阶段朗格汉斯细胞(LC)的数量和抗原呈递能力。诱导前,口腔黏膜和皮肤中F4/80 + 主要组织相容性复合体(MHC)II类 + LC的数量无显著差异。诱导后,F4/80 + MHC II类 + LC数量增加,但口腔黏膜中的增加明显小于皮肤。对给予抗CD86抗体的小鼠进行的MEST显示,口服黏膜或皮肤致敏后耳肿胀均受到类似抑制。在口服黏膜致敏后的DTH小鼠模型中,诱导后F4/80 + CD86 + LC数量增加,但增加明显小于皮肤致敏后的DTH小鼠模型。本研究表明,在DTH小鼠模型中,口服黏膜致敏引发的反应比皮肤致敏弱。这可能是因为口服黏膜致敏诱导的LC较少,导致抗原呈递能力较低。

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Acta Odontol Scand. 2001 Aug;59(4):248-54. doi: 10.1080/00016350152509283.
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Ann N Y Acad Sci. 1996 Feb 13;778:1-27. doi: 10.1111/j.1749-6632.1996.tb21110.x.

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