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Status |
Public on May 17, 2019 |
Title |
Immune Checkpoint Regulation of Pulmonary Fibrosis [bulk RNA-seq] |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
|
Summary |
Fibroblasts from idiopathic pulmonary fibrosis (IPF) patients acquire an invasive phenotype that is essential for progressive fibrosis. The immune checkpoint ligand CD274 (PD-L1) is up-regulated on invasive lung fibroblasts, regulated by P53 and FAK signaling, and drives lung fibrosis in a humanized IPF model in mice. Targeting CD274high fibroblasts blunted invasion in vitro and attenuated fibrosis in vivo, suggesting that CD274 may be a novel therapeutic target in IPF.
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Overall design |
Reveal of the expression of the checkpoint PD1 ligand CD274 in invasive and non-invasive fibroblasts of both normal human lungs and IPF lungs
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Contributor(s) |
Geng Y, Liu X, Liang J, Deng N, Wang Y, Jiang D, Noble PW |
Citation(s) |
30763282, 35980387 |
Submission date |
Aug 22, 2018 |
Last update date |
Oct 26, 2022 |
Contact name |
AGCT Core |
Organization name |
Cedars Sinai Medical Center
|
Department |
BMS
|
Street address |
8687 Melrose Ave, PDC B230
|
City |
West Hollywood |
State/province |
CA |
ZIP/Postal code |
90069 |
Country |
USA |
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Platforms (1) |
GPL21290 |
Illumina HiSeq 3000 (Homo sapiens) |
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Samples (18)
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Relations |
BioProject |
PRJNA487358 |
SRA |
SRP158619 |