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CD8+ T 细胞在小鼠模型中介导阿莫西林皮肤过敏。

CD8+ T cells mediate skin allergy to amoxicillin in a mouse model.

机构信息

Université Lyon 1, UFR Lyon Sud, Pierre-Bénite, France.

出版信息

Allergy. 2010 Aug;65(8):996-1003. doi: 10.1111/j.1398-9995.2009.02307.x. Epub 2010 Feb 1.

Abstract

BACKGROUND

Delayed allergic skin reactions to drugs are common iatrogenic diseases mediated by activation of specific T cells in the skin.

METHODS

To better understand the role of T cells in these diseases, we developed a mouse model of drug allergy induced by skin sensitization to amoxicillin (amox), a penicillin antibiotic frequently involved in delayed drug allergy.

RESULTS

Whereas wild-type mice could not be sensitized to amox, CD4+ T-cell-deficient mice developed an amox-specific allergic skin response, mediated by IFN-gamma-producing CD8+ T cells. Amox-specific CD8+ T cells, induced in lymphoid organs at a high frequency during sensitization, were recruited in the skin upon challenge. CD8+ T cells were effectors of the allergic skin reaction to amox as in vivo treatment with depleting anti-CD8 mAbs abrogated the skin inflammatory reaction and as purified CD8+ T cells could adoptively transfer the allergic response to naive recipients.

CONCLUSION

CD8+ T cells mediate penicillin skin allergy.

摘要

背景

药物迟发性过敏皮肤反应是由皮肤中特定 T 细胞激活引起的常见医源性疾病。

方法

为了更好地了解 T 细胞在这些疾病中的作用,我们建立了一种通过对青霉素类抗生素阿莫西林(amox)致敏诱导的药物过敏的小鼠模型。

结果

虽然野生型小鼠不能对 amox 致敏,但 CD4+T 细胞缺陷型小鼠会产生由 IFN-γ产生的 CD8+T 细胞介导的 amox 特异性过敏皮肤反应。在致敏过程中,淋巴器官中高频率诱导的 amox 特异性 CD8+T 细胞在受到挑战时会募集到皮肤中。CD8+T 细胞是对 amox 过敏皮肤反应的效应物,因为体内用耗竭性抗 CD8 mAb 治疗可消除皮肤炎症反应,并且纯化的 CD8+T 细胞可以将过敏反应转移给未致敏的受体。

结论

CD8+T 细胞介导青霉素皮肤过敏。

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