Fahy John V
Division of Pulmonary and Critical Care Medicine and the Cardiovascular Research Institute, Room 1307, Health Sciences East, 513 Parnassus Avenue, San Francisco, California 94143, USA.
Nat Rev Immunol. 2015 Jan;15(1):57-65. doi: 10.1038/nri3786.
Asthma is one of the most common chronic immunological diseases in humans, affecting people from childhood to old age. Progress in treating asthma has been relatively slow and treatment guidelines have mostly recommended empirical approaches on the basis of clinical measures of disease severity rather than on the basis of the underlying mechanisms of pathogenesis. An important molecular mechanism of asthma is type 2 inflammation, which occurs in many but not all patients. In this Opinion article, I explore the role of type 2 inflammation in asthma, including lessons learnt from clinical trials of inhibitors of type 2 inflammation. I consider how dichotomizing asthma according to levels of type 2 inflammation--into 'T helper 2 (TH2)-high' and 'TH2-low' subtypes (endotypes)--has shaped our thinking about the pathobiology of asthma and has generated new interest in understanding the mechanisms of disease that are independent of type 2 inflammation.
哮喘是人类最常见的慢性免疫疾病之一,影响着从儿童到老年的人群。哮喘治疗进展相对缓慢,治疗指南大多基于疾病严重程度的临床指标推荐经验性方法,而非基于发病机制的潜在机制。哮喘的一个重要分子机制是2型炎症,许多但并非所有患者都会出现这种炎症。在这篇观点文章中,我探讨了2型炎症在哮喘中的作用,包括从2型炎症抑制剂临床试验中吸取的经验教训。我思考了根据2型炎症水平将哮喘分为“2型辅助性T细胞(TH2)高”和“TH2低”亚型(内型)如何塑造了我们对哮喘病理生物学的认识,并引发了对理解独立于2型炎症的疾病机制的新兴趣。