National Heart and Lung Institute, Imperial College, London, UK.
Immunol Rev. 2011 Jul;242(1):31-50. doi: 10.1111/j.1600-065X.2011.01020.x.
Allergic inflammation is due to a complex interplay between several inflammatory cells, including mast cells, basophils, lymphocytes, dendritic cells, eosinophils, and sometimes neutrophils. These cells produce multiple inflammatory mediators, including lipids, purines, cytokines, chemokines, and reactive oxygen species. Allergic inflammation affects target cells, such as epithelial cells, fibroblasts, vascular cells, and airway smooth muscle cells, which become an important source of inflammatory mediators. Sensory nerves are sensitized and activated during allergic inflammation and produce symptoms. Allergic inflammatory responses are orchestrated by several transcription factors, particularly NF-κB and GATA3. Inflammatory genes are also regulated by epigenetic mechanisms, including DNA methylation and histone modifications. There are several endogenous anti-inflammatory mechanisms, including anti-inflammatory lipids and cytokines, which may be defective in allergic disease, thus amplifying and perpetuating the inflammation. Better understanding of the pathophysiology of allergic inflammation has identified new therapeutic targets but developing effective novel therapies has been challenging. Corticosteroids are highly effective with a broad spectrum of anti-inflammatory effects, including epigenetic modulation of the inflammatory response and suppression of GATA3.
过敏炎症是由多种炎症细胞（包括肥大细胞、嗜碱性粒细胞、淋巴细胞、树突状细胞、嗜酸性粒细胞，有时还有中性粒细胞）之间的复杂相互作用引起的。这些细胞产生多种炎症介质，包括脂质、嘌呤、细胞因子、趋化因子和活性氧。过敏炎症会影响靶细胞，如上皮细胞、成纤维细胞、血管细胞和气道平滑肌细胞，这些细胞成为炎症介质的重要来源。在过敏炎症期间，感觉神经会被致敏和激活，并产生症状。过敏炎症反应由几种转录因子（特别是 NF-κB 和 GATA3）协调。炎症基因也受到表观遗传机制的调控，包括 DNA 甲基化和组蛋白修饰。存在几种内源性抗炎机制，包括抗炎脂质和细胞因子，它们在过敏疾病中可能存在缺陷，从而放大和持续炎症。更好地了解过敏炎症的病理生理学已经确定了新的治疗靶点，但开发有效的新型治疗方法具有挑战性。皮质类固醇具有广泛的抗炎作用，包括对炎症反应的表观遗传调节和对 GATA3 的抑制作用，因此非常有效。
