IL-33 induces production of autoantibody against autologous respiratory epithelial cells: a potential mechanism for the pathogenesis of COPD

Immunology
Qin LiSun Ying

Abstract

The mechanisms underlying the chronic, progressive airways inflammation, remodelling and alveolar structural damage characteristic of human chronic obstructive pulmonary disease (COPD) remain unclear. In the present study, we address the hypothesis that these changes are at least in part mediated by respiratory epithelial alarmin (IL-33)-induced production of autoantibodies against airways epithelial cells. Mice immunized with homologous, syngeneic lung tissue lysate along with IL-33 administered directly to the respiratory tract or systemically produced IgG autoantibodies binding predominantly to their own alveolar type II epithelial cells, along with increased percentages of Tfh cells and B2 B-cells 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 II epithelial cells, suggesting specificity for common, cross-species determinants. Finally, concentrations of antibodies against both human and murine alveolar epithelial cells were significantl...Continue Reading

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Citations

Dec 10, 2020·The Journal of International Medical Research·Xia XuHongyu Zhang
Feb 2, 2021·Immunological Investigations·Faezeh RamezaniHamed Mohammadi
Dec 4, 2020·International Journal of Molecular Sciences·Julio Flores-GonzalezLeslie Chavez-Galan
Jan 19, 2020·Cellular Signalling·Stefan HadzicDjuro Kosanovic
Apr 8, 2020·ACS Pharmacology & Translational Science·Chantal Donovan, Philip M Hansbro

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