@article {Zhou2000404, author = {Zhou, Jie-Sen and Li, Zhou-Yang and Xu, Xu-Chen and Zhao, Yun and Wang, Yong and Chen, Hai-Pin and Zhang, Min and Wu, Yin-Fang and莱，天港和迪，春宁和董，ling-ling和刘，胡安和Xuan，nan-xia和Zhu，chen and wu，yan-ping and yan-ping和huang，hua-qiong and yan and yan and yan，fu-gui和fu-gui和fu-gui and and and and and and and and and and and and and and and and and and and and and and and and and and and and and和Hua，Wen和Wang，Yi和Xiong，Wei-ning和Qiu，Hui和Chen，Tao和Weng，Dong和Li，Hui-Ping和Zhou，Xiaobo和Wang，Lie and Liu and Liu，Fang and Lin，Xin and Ying，Xin and Ying，Ying，Ying，Ying，Ying，Ying，Ying，Ying，Ying，Ying，Ying，ying，ying，ying，ying，ying，ying，ying，ying，ying，ying，ying，ying，ying，lin and ying，lin and ying，lin and ying，lin and ying，lin and ying，lin and ying，linSong-Min和Li，Wen和Imamura，Mitsuru和Choi，Mary E.和Stampfli，Martin R.和Choi，Augustine M.K.以及陈，Zhi-hua和Shen，Hua-Hao}，title = {香烟引发的自身免疫性促进对小鼠中弹性蛋白诱导的类似COPD的病理的敏感性，体积= {56}id = {2000404}，年= {2020}，doi = {10.1183/13993003.00404-2020}，发行者= {欧洲呼吸社会}，摘要= {目188bet官网地址前尚不了解香烟烟雾是否促进对自我抗原和是否促进自我抗原的敏感性随之而来的自身反应性T细胞驱动慢性阻塞性肺疾病（COPD）相关的病理。为了解决这个问题，小鼠暴露于香烟烟雾中2周。在经历了2周的休息之后，小鼠被弹性蛋白肠内挑战3天或1个月。RAG1 - / - ，MMP12 - / - 和IL17A - / - 小鼠和针对活性弹性蛋白片段的中和抗体用于机械研究。人类GVAPGVGVAPGV/HLA-A*02：01四聚体合成以评估COPD患者的弹性蛋白特异性T细胞的存在。我们观察到2周的香烟烟雾暴露会导致弹性弹性的T细胞反应，从而导致中性粒细胞粒细胞嗜中性粒细胞嗜中性粒细胞粒细胞。 inflammation and mucus hyperproduction following elastin recall challenge. Repeated elastin challenge for 1 month resulted in airway remodelling, lung function decline and airspace enlargement. Elastin-specific T cell recall responses were dose dependent and memory lasted for over 6 months. Adoptive T cell transfer and studies in T cells deficient Rag1-/-mice conclusively implicated T cells in these processes. Mechanistically, cigarette smoke exposure-induced elastin-specific T cell responses were matrix metalloproteinase (MMP)12-dependent, while the ensuing immune inflammatory processes were interleukin 17A-driven. Anti-elastin antibodies and T cells specific for elastin peptides were increased in patients with COPD.These data demonstrate that MMP12-generated elastin fragments serve as a self-antigen and drive the cigarette smoke-induced autoimmune processes in mice that result in a bronchitis-like phenotype and airspace enlargement. The study provides proof of concept of cigarette smoke-induced autoimmune processes and may serve as a novel mouse model of COPD.MMP12-generated elastin fragments serve as a self-antigen and drive cigarette smoke-induced autoimmune processes in mice. These findings provide experimental evidence for cigarette smoke-induced autoimmunity and represent a novel mouse model of COPD. https://bit.ly/2XK9dC6}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/56/3/2000404}, eprint = {//www.qdcxjkg.com/content/56/3/2000404.full.pdf}, journal = {European Respiratory Journal} }