IL-33 and IL-9–producing innate immune cells in lung injury after pediatric bone marrow transplant
IL-33 induced-lL-9 producing type 2 innate lymphoid cells in the regulation of acute lung injury after hematopoietic stem cell transplantation (HSCT) in pediatric patients
Researchers are looking at how an immune signal called IL-33 and certain immune cells that make IL-9 affect lung injury in children after allogeneic stem cell (bone marrow) transplants.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Medical University of South Carolina NIH-funded |
| Lab location | 1 site (Charleston, United States) |
| Project ID | NIH-11017702 on NIH RePORTER |
What this research studies
This work links blood and lung samples from children who received allogeneic hematopoietic stem cell transplants with laboratory experiments to track IL-33, its decoy receptor sST2, IL-9, and specific type 2 innate lymphoid cells. Researchers will measure these molecules in patient samples and use cell and animal models to see how the signals change lung inflammation and damage. The team builds on prior biomarker findings (sST2) and aims to connect those markers to a clear immune mechanism that may drive idiopathic pneumonia syndrome after transplant. Findings will be used to search for ways to predict, prevent, or treat noninfectious acute lung injury after pediatric HSCT.
Who could benefit from this research
Good fit: Children who have received or will receive allogeneic hematopoietic stem cell transplantation and who are at risk for or developing noninfectious acute lung injury/idiopathic pneumonia syndrome are the ideal candidates to contribute samples or participate in related studies.
Not a fit: People without a history of bone marrow/stem cell transplant, adults, or patients whose lung problems are clearly caused by infection are unlikely to benefit directly from this specific project.
Why it matters
Potential benefit: If successful, this work could lead to better blood or lung markers to spot children at high risk for post-transplant lung failure and suggest targets for new treatments to prevent or reduce lung injury.
How similar studies have performed: Previous work from this group identified sST2 as a biomarker linked to transplant lung complications, but the role of IL-33–driven IL-9–producing ILC2 cells in this setting is a newer, less-tested mechanism.
Where this research is happening
Charleston, United States
- Medical University of South Carolina — Charleston, United States (Active)
Researchers
- Principal investigator: Paczesny, Sophie — Medical University of South Carolina
- Study coordinator: Paczesny, Sophie
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.