Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany.
Curr Opin Allergy Clin Immunol. 2010 Oct;10(5):463-8. doi: 10.1097/ACI.0b013e32833e3163.
We review here the recent discoveries in innate immunity that shed light on the pathophysiology of atopic dermatitis.
The mechanisms that promote the enhanced susceptibility to cutaneous infections in atopic dermatitis are complex interactions among several factors. They include skin barrier dysfunction, reduced skin lipid content, and abnormalities of the innate immune response. Some of the innate immune defects observed in atopic dermatitis are primary defects, such as epithelial barrier defects and defects in signaling or expression of innate receptors. Others may be secondary to the effects of the adaptive immune response. For example, deficiencies in antimicrobial peptides may be due to the overexpression of T helper 2 cytokines such as interleukin-4 and interleukin-13. However, how all components interact with each other remains to be fully investigated.
To break this vicious circle, a multiprolonged approach directed at healing or protecting the skin barrier and addressing the immune dysregulation is necessary to improve and control the disease.
本文综述了固有免疫的最新发现，这些发现阐明了特应性皮炎的病理生理学机制。
导致特应性皮炎患者更易发生皮肤感染的机制是多种因素的复杂相互作用。这些因素包括皮肤屏障功能障碍、皮肤脂质含量减少以及固有免疫反应异常。特应性皮炎中观察到的一些固有免疫缺陷是原发性缺陷，例如上皮屏障缺陷以及固有受体信号转导或表达缺陷。其他缺陷可能继发于适应性免疫反应的影响。例如，抗菌肽的缺乏可能是由于白细胞介素 4 和白细胞介素 13 等辅助性 T 细胞 2 细胞因子的过度表达所致。然而，所有这些成分如何相互作用仍有待充分研究。
要打破这种恶性循环，需要采用多方面的长期方法来修复或保护皮肤屏障，并解决免疫失调问题，以改善和控制疾病。
