Language

English

Publication Date

9-24-2025

Journal

Communications Biology

DOI

10.1038/s42003-025-08698-1

PMID

40993192

PMCID

PMC12460644

PubMedCentral® Posted Date

9-24-2025

PubMedCentral® Full Text Version

Post-print

Abstract

There is a significant knowledge gap in how T cells promote emphysema in smokers with chronic obstructive pulmonary disease (COPD). Single-cell RNA sequencing (scRNA seq) analysis of human samples and relevant clinical data can provide new mechanistic insights into disease pathogenesis. We generated a human lung scRNA seq dataset with extensive disease characteristic annotation and analyzed a second independent scRNA seq dataset to examine the pathophysiological role of T cells in emphysema. Comparisons of pulmonary immune landscapes in emphysematous (E)-COPD, non-emphysematous (NE)-COPD, and control showed positive enrichment of T cells in E-COPD. Pathway analyses identified upregulated inflammatory states in CD4 T cells as a distinguishing feature of E-COPD. Compared to controls, glucocorticoid receptor NR3C1 CD4 T cells were enriched in NE-COPD but were reduced in E-COPD. Interactions between macrophages and NR3C1+ CD4 T cell subsets via CXCL signaling were strongly predicted in E-COPD but were absent in NE-COPD and control. The relative abundance of CD4 CXCR6high effector memory T cells positively correlated with preserved lung function in E-COPD but not in NE-COPD. These findings suggest that NR3C1+ and CXCR6high effector memory subsets of CD4 T cells distinguish the immune-pathophysiological features of emphysema in human lungs. Targeting relevant T cell subsets in emphysema might provide new therapeutic opportunities.

Keywords

Humans, Lung, Pulmonary Emphysema, Receptors, CXCR6, Receptors, Glucocorticoid, Pulmonary Disease, Chronic Obstructive, Male, CD4-Positive T-Lymphocytes, Female, Middle Aged, Aged, Single-Cell Analysis, Chronic inflammation, Predictive markers

Published Open-Access

yes

42003_2025_8698_Figa_HTML.jpg (141 kB)
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