How airway cells and immune T cells cause long-term damage after lung transplant
Airway epithelial cell and lymphocyte interactions in chronic lung allograft dysfunction pathogenesis
This project looks at how the airway lining and immune T cells interact to cause chronic lung transplant damage in people who have received lung transplants.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California, San Francisco NIH-funded |
| Lab location | 1 site (San Francisco, United States) |
| Project ID | NIH-11390619 on NIH RePORTER |
What this research studies
Researchers will collect small airway brush samples from lung transplant recipients at several transplant centers and study gene activity where chronic lung allograft dysfunction (CLAD) starts. In the lab they will expose airway cells to low-oxygen conditions to see how those cells attract and activate cytotoxic T lymphocytes and trigger cell-death pathways. The team will compare these airway transcriptomes and immune signals across patients and centers to identify consistent pathways such as hypoxia signaling and TNF-family genes. Findings are intended to reveal early molecular signals that could be targeted to prevent airway scarring after transplant.
Who could benefit from this research
Good fit: Ideal candidates are lung transplant recipients who can provide small airway brush samples or participate through the participating transplant programs.
Not a fit: People without a lung transplant and those seeking an immediate treatment should not expect direct clinical benefit from this lab-focused, observational study.
Why it matters
Potential benefit: If successful, this work could point to early molecular targets to prevent or slow CLAD, improving long-term lung transplant function and quality of life.
How similar studies have performed: Previous multi-center airway transcriptome studies from these groups have found gene signatures tied to CLAD and preliminary lab models support roles for hypoxia and TNF-family pathways, but translation to therapies is still early.
Where this research is happening
San Francisco, United States
- University of California, San Francisco — San Francisco, United States (Active)
Researchers
- Principal investigator: Greenland, John — University of California, San Francisco
- Study coordinator: Greenland, John
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.