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Contact sensitivity in the murine oral mucosa. I. An experimental model of delayed-type hypersensitivity reactions at mucosal surfaces.

机译:鼠口腔粘膜的接触敏感性。 I.在粘膜表面的迟发型超敏反应的实验模型。

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摘要

We have examined in a murine model, the potential of the oral mucosa (OM) to serve as inductive and/or expression site(s) of delayed-type hypersensitivity (DTH) reactions. The expression of DTH reactions in the murine buccal mucosa was studied after topical application of oxazolone or picryl chloride onto the OM of animals previously sensitized with either hapten. Irrespective of the site of priming (skin or buccal mucosa), inflammatory cells appeared in the OM following buccal elicitation with the pertinent hapten. The density of infiltrating cells peaked at 24 h after hapten elicitation. Such inflammatory reactions, which comprised mainly mononuclear cells at 24 h, were preceded by an early inflammatory reaction that developed only in animals previously sensitized at skin sites. This early reaction, comprising mainly PMN neutrophils, peaked at 6-8 h, declined by 8-16 h, and was not observed in mice previously sensitized in the buccal mucosa. The 24 h reactions failed to develop in nude mice similarly treated, in intact unsensitized mice, as well as in animals sensitized with an irrelevant hapten. These reactions could be adoptively transferred to naive animals by LN cells but not by serum from sensitized syngeneic donors. Furthermore, LN cell suspensions depleted of T cells failed to transfer sensitization for subsequent OM DTH. Topical application of contact sensitizing haptens onto OM induced priming for subsequent DTH reactions elicited with recall antigen applied at a distant skin site or at a local buccal site. These results demonstrate that the OM has the capacity to serve both as an inductive and as an expression site for T cell-mediated inflammatory reactions, be these expressed or induced at local mucosal sites or at remote systemic (skin) sites. This animal model should be valuable for studying the regulation of T cell-mediated inflammatory responses at mucosal surfaces.
机译:我们已经在鼠模型中检查了口腔粘膜(OM)用作延迟型超敏反应(DTH)反应的诱导和/或表达位点的潜力。在将恶唑酮或氯化苦味素局部应用到先前用两种半抗原致敏的动物的OM上后,研究了DTH反应在鼠颊粘膜中的表达。不论引发部位(皮肤或颊粘膜)如何,在与相关的半抗原一起颊颊诱发后,OM中都会出现炎症细胞。在半抗原诱导后24小时,浸润细胞的密度达到峰值。此类炎症反应主要在24 h处包含单核细胞,随后发生早期炎症反应,这种炎症反应仅在先前在皮肤部位敏化的动物中发生。这种早期反应主要包括PMN中性粒细胞,在6-8小时达到峰值,在8-16小时下降,并且在先前在颊粘膜中致敏的小鼠中未观察到。在经过同样处理的裸鼠,完整的未敏化小鼠以及被无关的半抗原致敏的动物中,24小时反应未能发展。这些反应可以通过LN细胞过继转移到幼稚动物身上,而不是通过致敏同系供体的血清过继转移到幼稚动物身上。此外,耗尽T细胞的LN细胞悬液无法转移对后续OM DTH的敏化作用。对于在远处皮肤部位或局部颊部位施加的召回抗原引起的后续DTH反应,将接触致敏半抗原局部应用到OM诱导的引发中。这些结果证明,OM具有作为T细胞介导的炎症反应的诱导位点和表达位点的能力,无论是在局部粘膜位点还是在远端全身(皮肤)位点表达或诱导的。这种动物模型对于研究粘膜表面T细胞介导的炎症反应的调控是有价值的。

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