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In the present study, we address the hypothesis that these changes are at least in part mediated by respiratory epithelial alarmin (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033)\u2010induced production of autoantibodies against airways epithelial cells. Mice immunized with homologous, syngeneic lung tissue lysate along with <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 administered directly to the respiratory tract or systemically produced IgG autoantibodies binding predominantly to their own alveolar type <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> epithelial cells, along with increased percentages of Tfh cells and B2 B\u2010cells in their local, mediastinal lymph nodes. Consistent with its specificity for respiratory epithelial cells, this autoimmune inflammation was confined principally to the lung and not other organs such as the liver and kidney. Furthermore, the serum autoantibodies produced by the mice bound not only to murine, but also to human alveolar type <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> epithelial cells, suggesting specificity for common, cross\u2010species determinants. Finally, concentrations of antibodies against both human and murine alveolar epithelial cells were significantly elevated in the serum of patients with <jats:styled-content style=\"fixed-case\">COPD<\/jats:styled-content> compared with those of control subjects. These data are consistent with the hypothesis that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 contributes to the chronic, progressive airways obstruction, inflammation and alveolar destruction characteristic of phenotypes of <jats:styled-content style=\"fixed-case\">COPD<\/jats:styled-content>\/emphysema through induction of\u00a0autoantibodies against lung tissue, and particularly alveolar type <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> epithelial cells.<\/jats:p>","DOI":"10.1111\/imm.13054","type":"journal-article","created":{"date-parts":[[2019,2,26]],"date-time":"2019-02-26T04:39:14Z","timestamp":1551155954000},"page":"137-150","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["<scp>IL<\/scp>\u201033 induces production of autoantibody against autologous respiratory epithelial cells: a potential mechanism for the pathogenesis of <scp>COPD<\/scp>"],"prefix":"10.1111","volume":"157","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3640-8625","authenticated-orcid":false,"given":"Qin","family":"Li","sequence":"first","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yue","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhe","family":"Lv","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jingjing","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Laboratory Animal Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3812-7192","authenticated-orcid":false,"given":"Gao","family":"An","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaonan","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huating","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine Beijing Chao\u2010Yang Hospital Capital Medical University &amp; Beijing Institute of Respiratory Medicine Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chris J.","family":"Corrigan","sequence":"additional","affiliation":[{"name":"Faculty of Life Sciences &amp; Medicine School of Immunology &amp; Microbial Sciences Asthma UK Centre in Allergic Mechanisms of Asthma King's College London London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sun","family":"Ying","sequence":"additional","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Capital Medical University Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2019,3,27]]},"reference":[{"key":"e_1_2_8_2_1","unstructured":"Global Initiative for Chronic Obstructive Lung Disease. 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