PDF(Pubmed)
Abstract：
Type 2 inflammation is characterized by overexpression and heightened activity of type 2 cytokines, mediators, and cells that drive neuroimmune activation and sensitization to previously subthreshold stimuli. The consequences of altered neuroimmune activity differ by tissue type and disease; they include skin inflammation, sensitization to pruritogens, and itch amplification in atopic dermatitis and prurigo nodularis; airway inflammation and/or hyperresponsiveness, loss of expiratory volume, airflow obstruction and increased mucus production in asthma; loss of sense of smell in chronic rhinosinusitis with nasal polyps; and dysphagia in eosinophilic esophagitis. We describe the neuroimmune interactions that underlie the various sensory and autonomic pathologies in type 2 inflammatory diseases and present recent advances in targeted treatment approaches to reduce type 2 inflammation and its associated symptoms in these diseases. Further research is needed to better understand the neuroimmune mechanisms that underlie chronic, sustained inflammation and its related sensory pathologies in diseases associated with type 2 inflammation.
摘要：
2型炎症的特征是2型细胞因子的过度表达和活性增强。驱动神经免疫激活和对先前亚阈值刺激敏感的介质和细胞。神经免疫活性改变的后果因组织类型和疾病而异，包括：皮肤炎症，致敏剂，特应性皮炎和结节性痒疹的瘙痒放大；气道炎症/高反应性，呼气量损失,哮喘的气流阻塞和粘液产生增加；慢性鼻-鼻窦炎伴鼻息肉的嗅觉丧失；嗜酸性粒细胞性食管炎的吞咽困难。我们描述了作为2型炎症性疾病中各种感觉和自主神经病理基础的神经免疫相互作用，并提出了在这些疾病中减少2型炎症及其相关症状的靶向治疗方法的最新进展。需要进一步的研究来更好地了解慢性疾病的神经免疫机制，2型炎症相关疾病的持续炎症及其相关的感觉病理。
