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Paper

Single-cell dissection of chronic lung allograft dysfunction reveals convergent and distinct fibrotic mechanisms

Evidence level: single-cell transcriptomic analysis of explanted lungs with cross-disease integration; abstract-only

A single-cell analysis of CLAD lungs integrated with data from other fibrotic lung diseases, reporting CLAD-specific cell subsets and a shared KRT17-positive, KRT5-negative cell population.

As of . Primary source: Publisher record via DOI.

Summary

The abstract describes a single-cell transcriptomic analysis of CLAD lungs that combined newly generated datasets with about 1.6 million cells from 15 published studies of other fibrotic lung diseases. The authors report CLAD-specific cell subsets, namely Fibro.AT2 cells, exhausted CD8 T cells and superactivated macrophages, and suggest that KRT17-positive, KRT5-negative cells represent a common fibrotic mechanism across fibrotic lung diseases. A donor and recipient cell deconvolution found that recipient-derived stromal and immune cells showed stronger pro-fibrotic and allograft rejection pathways than donor-derived counterparts. The authors present this as a molecular framework and a source of potential therapeutic targets. The numbers of patients are not stated in the abstract.

Details

doi
10.1172/jci.insight.197579
pmid
41122970
authors
Yan Y, Kaihou T, Lecuona E, Wu X, Shigemura M, Sun H, Kurihara C, Gao R, Nunez-Santana FL, Budinger GS, Bharat A
journal
JCI Insight
year
2025
volume
10
issue
20
articleNumber
e197579

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Information resource only. Not medical advice. Not a substitute for the care of the patient's transplant team.