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斑丘疹性皮疹的分子机制

Molecular mechanisms of maculopapular exanthema.

作者信息

Fernández Tahia D, Canto Gabriela, Blanca Miguel

机构信息

Research Laboratory for Allergic Diseases, Carlos Haya Hospital-Fundacion IMABIS, Malaga, Spain.

出版信息

Curr Opin Infect Dis. 2009 Jun;22(3):272-8. doi: 10.1097/QCO.0b013e3283298e62.

Abstract

PURPOSE OF REVIEW

Maculopapular exanthema is a common cutaneous manifestation of many diseases produced by several agents able to activate the immune system, the most common of which are drugs and viruses. In spite of its high frequency, knowledge of the molecular mechanisms involved remains scarce.

RECENT FINDINGS

The cytokine patterns in maculopapular exanthema have a Th1 or Th0 pattern, according to whether the reaction is induced by a drug or a virus, respectively. Additionally, the involvement of CD4 T-lymphocytes with cytotoxic capabilities has been shown in the former. Different chemokines and their receptors are also involved in skin homing, such as CCL20, CCL27, CXCL9 or CXCL10, and oxidative stress can help exacerbate the symptoms.

SUMMARY

These findings may be very important for the diagnostic evaluation of these entities and for the development of new tools for diagnosis and treatment.

摘要

综述目的

斑丘疹是由多种能够激活免疫系统的病原体引发的许多疾病常见的皮肤表现,其中最常见的是药物和病毒。尽管其发病率很高,但对其相关分子机制的了解仍然很少。

最新发现

根据反应是由药物还是病毒诱导,斑丘疹中的细胞因子模式分别具有Th1或Th0模式。此外,前者已显示具有细胞毒性能力的CD4 T淋巴细胞参与其中。不同的趋化因子及其受体也参与皮肤归巢,如CCL20、CCL27、CXCL9或CXCL10,氧化应激可加剧症状。

总结

这些发现对于这些疾病的诊断评估以及开发新的诊断和治疗工具可能非常重要。

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