RT期刊文章SR电子T1 IL-22及其受体在人类和实验性COPD中增加，并有助于发病机理JF欧洲呼吸杂志Jo Eur Respir J FD欧洲呼吸学会SP 1800174 DO 10.1183/13993003.0033003.00174-2018188bet官网地址Malcolm R. A1木板，Maximilian W. A1 Casolari，Paolo A1 Papi，Alberto A1 Pavlidis，Stelios A1 Guo，Yike A1 Cameron，Guy J.M. A1 Haw，Tatt Jhong A1 Tam，Anthony A1 Tam，Anthony A1 obiedat，Ma'en A1 Donovan，Chantal A11Hansbro，Nicole G. A1 Nguyen，Duc H. A1 Nair，Prema Mono A1 Kim，Richard Y. A1 Horvat，Jay C. A1 Kaiko，Gerard E. A1 Durum，Scott K. A1 Wark，Peter A. A1 Sin，Don，Don，Don，DonD. A1 Caramori，Gaetano A1 Adcock，Ian M. A1 Foster，Paul S. A1 Hansbro，Philip M. YR 2019 UL //www.qdcxjkg.com/content.com/content/54/18001/1800174.4.abstract疾病（COPD）是全球发病和死亡的第三主要原因。缺乏有效的治疗方法是由于对驱动COPD发病机制的基本机制的不完全理解。Interleukin（IL）-22与气道炎症有关，COPD患者增加。但是，其在COPD发病机理中的作用知之甚少。在这里，我们研究了IL-22在人类COPD和香烟烟雾（CS）诱导的实验性COPD.IL-22和IL-22受体mRNA表达和蛋白质水平的作用，而健康吸烟或非健康吸烟或非 -吸烟控制。与对照组相比，用实验COPD的小鼠的肺中IL-22和IL-22受体水平升高，IL-22的细胞来源包括CD4+ T-助细胞，γδT细胞，γδT细胞，天然杀手T细胞和3组3先天淋巴样细胞。 CS-induced pulmonary neutrophils were reduced in IL-22-deficient (Il22−/−) mice. CS-induced airway remodelling and emphysema-like alveolar enlargement did not occur in Il22−/− mice. Il22−/− mice had improved lung function in terms of airway resistance, total lung capacity, inspiratory capacity, forced vital capacity and compliance.These data highlight important roles for IL-22 and its receptors in human COPD and CS-induced experimental COPD.IL-22 and its receptors are increased in both human and experimental chronic obstructive pulmonary disease (COPD). IL-22 drives neutrophilic inflammation and impaired lung function in experimental COPD. http://bit.ly/2Vsri6T