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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)
Verlagsversion DOI PMC
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 0903-1936
e-ISSN 1399-3003
Zeitschrift European Respiratory Journal
Quellenangaben Band: 62, Heft: 4, Seiten: , Artikelnummer: 14 Supplement: ,
Verlag European Respiratory Society
Verlagsort Sheffield
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Health and Immunity (LHI)
POF Topic(s) 30202 - Environmental Health
Forschungsfeld(er) Lung Research
PSP-Element(e) G-501600-005
G-501600-004
G-505000-007
Förderungen Bundesinstitut fur Risikoforschung (Federal Institute for Risk Assessment)
Deutsche Forschungsgemeinschaft (German Research Foundation)
German Center for Lung Research
DOI 10.1183/13993003.00589-2023
WOS ID 001085916200007
Scopus ID 85175468103
PubMed ID 37652569
Erfassungsdatum 2023-11-28
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