Ty -jour t1-烟雾引发的自身免疫性促进了小鼠中对弹性蛋白诱导的类似COPD的病理学的敏感性 - 欧洲呼吸杂志Zhou，Jie -sen au -li，Zhou -Yang au -Xu，Xu -chen au -Zhao，Yun au -Wang，Yong Au -Chen，Hai -pin au -Zhang -Zhang，Min au -Wu -wu，yin -fang au-- yin -fang au-莱，天王 - di，chun -hong au -dong，ling -ling au -liu，liu，juan au -xuan，nan -xia au -zhu -zhu，chen au -wu -yan -yan -ping au -yan -ping au -huang，hua -qiong，hua -qiongau -yan，fu -gui au -hua，wen au -wang，yi au -xiong，wei -ning au -qiu -qiu，hui au au -chen，tao au -weng -weng -weng，dong au -li- li，li，hui -ping au -ping au -zhou -zhou，zhou，zhou，zhou，Xiaobo au -Wang，Lie Au -Liu，Fang au -Lin，Xin au -ying，song -min au -li，li，wen au -imamura，Mitsuru au -choi -choi -choi，Mary E. au -apkfli -stampfli-，奥古斯丁M.K.Au -Chen，Zhi -hua au -shen，hua -hao y1-2020/09/01 ur -http：//www.qdcxjkg.com/content.com/content/56/3/3/2000404.4.Abstract n2 - 目前尚不理解是否不了解它是否不懂香烟烟雾暴露促进对自我抗原的敏感性以及随之而来的自身反应性T细胞是否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 ER -