Blockade of PD-1 decreases neutrophilic inflammation and lung damage in experimental COPD.
Animals
B7-H1 Antigen
/ antagonists & inhibitors
Disease Models, Animal
Female
Humans
Inflammation
/ metabolism
Lung
/ metabolism
Macrophages, Alveolar
/ metabolism
Male
Mice
Neutrophils
/ metabolism
Programmed Cell Death 1 Receptor
/ antagonists & inhibitors
Prospective Studies
Pulmonary Disease, Chronic Obstructive
/ metabolism
COPD
PD-1
PD-L1
inflammation
lung damage
macrophages
Journal
American journal of physiology. Lung cellular and molecular physiology
ISSN: 1522-1504
Titre abrégé: Am J Physiol Lung Cell Mol Physiol
Pays: United States
ID NLM: 100901229
Informations de publication
Date de publication:
01 05 2021
01 05 2021
Historique:
pubmed:
25
3
2021
medline:
28
7
2021
entrez:
24
3
2021
Statut:
ppublish
Résumé
Chronic obstructive lung disease (COPD) and lung cancer are both caused by smoking and often occur as comorbidity. The programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) axis is an important canonic immunoregulatory pathway, and antibodies that specifically block PD-1 or PD-L1 have demonstrated efficacy as therapeutic agents for non-small cell lung cancer. The role of the PD-1/PD-L1 axis in the pathogenesis of COPD is unknown. Here, we analyzed the function of the PD-1/PD-L1 axis in preclinical COPD models and evaluated the concentrations of PD-1 and PD-L1 in human serum and bronchoalveolar lavage (BAL) fluids as biomarkers for COPD. Anti-PD-1 treatment decreased lung damage and neutrophilic inflammation in mice chronically exposed to cigarette smoke (CS) or nontypeable
Identifiants
pubmed: 33759577
doi: 10.1152/ajplung.00121.2020
pmc: PMC8424521
doi:
Substances chimiques
B7-H1 Antigen
0
CD274 protein, human
0
Cd274 protein, mouse
0
PDCD1 protein, human
0
Pdcd1 protein, mouse
0
Programmed Cell Death 1 Receptor
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
L958-L968Références
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