CD55, a lung-protective protein, and how it may prevent smoke-related lung damage
Official title: Decay accelerating factor (CD55) protects against lectin pathway-mediated AT2 cell dysfunction in cigarette smoke-induced emphysema
Funded at University of Florida · NIH-11248766 · Data updated 2026-11-12
This project tests whether the protective protein CD55 can stop cigarette smoke from harming lung repair cells and slow emphysema in smokers and people with early COPD.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Florida NIH-funded |
| Lab location | 1 site (Gainesville, United States) |
| Project start | January 15, 2024 |
| Project end | December 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $587,175 |
| NIH project number | 5R01HL166828-04 |
| Project ID | NIH-11248766 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal participants would include current or former smokers and people with early-stage COPD who can provide blood samples or join translational biomarker studies.
✕Less likely to help
People with advanced or end-stage emphysema or unrelated lung conditions are less likely to benefit directly from this work.
What this research studies
This project looks at how cigarette smoke activates a part of the immune system called the lectin complement pathway to damage type 2 alveolar (AT2) cells that help repair air sacs. Researchers will identify which lectin pathway proteins drive complement to deposit on AT2 cells and use lab models of smoke exposure to study the resulting cell injury. They will test whether the cell-surface protector CD55 prevents complement from sticking to AT2 cells and helps those cells proliferate and change into the cells needed to rebuild air sacs. Finally, the team will develop a blood-based complement activity score from plasma proteins that could flag smokers and people with early COPD who are likely to progress toward emphysema.
Why it matters
Potential benefit: If successful, this work could yield blood tests to spot people at risk of emphysema earlier and point to ways to protect lung repair cells from smoke damage.
How similar studies have gone: Prior research links complement activity to lung injury, but targeting the lectin pathway and CD55 for preventing smoke-related emphysema is largely novel.
Where this research is happening
-
University of Florida
Gainesville, United States Active
Researchers
- Principal investigator: Serban, Karina — University of Florida
- Study coordinator: Serban, Karina
Related research
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A study to understand whether vaping or traditional cigarettes cause early lung damage in young adults.
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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.