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Kapellos, T. ; Conlon, T.M. ; Yildirim, A.Ö. ; Lehmann, M.

The impact of the immune system on lung injury and regeneration in COPD.

Eur. Respir. J. 62:14 (2023)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
COPD is a devastating respiratory condition that manifests via persistent inflammation, emphysema development and small airway remodelling. Lung regeneration is defined as the ability of the lung to repair itself after injury by the proliferation and differentiation of progenitor cell populations, and becomes impaired in the COPD lung as a consequence of cell intrinsic epithelial stem cell defects and signals from the micro-environment. Although the loss of structural integrity and lung regenerative capacity are critical for disease progression, our understanding of the cellular players and molecular pathways that hamper regeneration in COPD remains limited. Intriguingly, despite being a key driver of COPD pathogenesis, the role of the immune system in regulating lung regenerative mechanisms is understudied. In this review, we summarise recent evidence on the contribution of immune cells to lung injury and regeneration. We focus on four main axes: 1) the mechanisms via which myeloid cells cause alveolar degradation; 2) the formation of tertiary lymphoid structures and the production of autoreactive antibodies; 3) the consequences of inefficient apoptotic cell removal; and 4) the effects of innate and adaptive immune cell signalling on alveolar epithelial proliferation and differentiation. We finally provide insight on how recent technological advances in omics technologies and human ex vivo lung models can delineate immune cell-epithelium cross-talk and expedite precision pro-regenerative approaches toward reprogramming the alveolar immune niche to treat COPD.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Obstructive Pulmonary-disease; Smoke-induced Emphysema; Cell-activating Factor; Macrophage Phagocytic Function; Human Neutrophil Elastase; Cigarette-smoke; Alveolar Macrophages; Apoptotic Neutrophils; Tissue Inhibitor; Growth-factor
ISSN (print) / ISBN 0903-1936
e-ISSN 1399-3003
Journal European Respiratory Journal
Quellenangaben Volume: 62, Issue: 4, Pages: , Article Number: 14 Supplement: ,
Publisher European Respiratory Society
Publishing Place Sheffield
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Lung Health and Immunity (LHI)
Institute of Lung Biology (LHI)
Grants Bundesinstitut fur Risikoforschung (Federal Institute for Risk Assessment)
Deutsche Forschungsgemeinschaft (German Research Foundation)
German Center for Lung Research