IgA antibodies to oxidation-related targets in lung fibrosis
Official title: Oxidation-Specific Epitope IgA in Pulmonary Fibrosis
Funded at University of Virginia · NIH-11381817 · Data updated 2026-11-12
This NIH grant explores how certain IgA antibodies against damaged lung components relate to idiopathic pulmonary fibrosis and what that means for future therapies.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Virginia NIH-funded |
| Lab location | 1 site (Charlottesville, United States) |
| Project start | August 1, 2025 |
| Project end | May 31, 2030 |
| Funding year | 2026 |
| Award (this year) | $790,762 |
| NIH project number | 5R01HL179312-02 |
| Project ID | NIH-11381817 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with idiopathic pulmonary fibrosis or related lung conditions, and blood samples from IPF patients.
✕Less likely to help
Healthy individuals without IPF may not directly benefit, though insights could inform broader lung disease research.
What this research studies
IPF is a serious lung disease with unclear causes. The project looks at how B cells and IgA antibodies interact with oxidation-related targets in the lungs and whether these signals drive fibrosis. Researchers will use high-dimensional immune profiling to find a B cell subset linked to disease markers and may identify new therapeutic opportunities. The work translates to patients by pinpointing immune pathways that could be targeted to slow or halt lung scarring.
Why it matters
Potential benefit: If successful, findings could lead to new immune-based therapies for IPF.
How similar studies have gone: Prior work shows immune dysregulation and autoantibodies in IPF, with a potential for novel targets in this project.
Where this research is happening
-
University of Virginia
Charlottesville, United States Active
Researchers
- Principal investigator: Sturek, Jeffrey Michael — University of Virginia
- Study coordinator: Sturek, Jeffrey Michael
Related research
Other NIH-funded projects on the same topics.
-
Molecular clues to progressive lung scarring
Researchers are studying how lung tissue becomes progressively scarred, focusing on cell signals and receptors that may drive fibrosis in people with lung disease.
-
Alveolar Cell Dysfunction in Pulmonary Fibrosis: Using SFTPC Mutations to Find New Targets
This grant explores how rare SFTPC mutations in alveolar cells may drive IPF and seeks new molecular targets to improve treatment.
-
Iron and scar-forming cells in the lungs (IPF)
Researchers are exploring how iron in the lungs may drive the scarring seen in idiopathic pulmonary fibrosis and whether this could lead to new therapies.
-
Repurposing Pyrvinium as an Inhaled Therapy for Idiopathic Pulmonary Fibrosis
A patient-friendly look at a project trying to use an existing drug, pyrvinium, as an inhaled treatment option for idiopathic pulmonary fibrosis (IPF).
-
Screening new compounds to reverse gene signatures in IPF lungs
A researcher hopes to find compounds that reverse harmful gene changes in the lungs of people with idiopathic pulmonary fibrosis (IPF).
-
Role of lactate transporters in lung scarring
Aims to see if blocking lactate transporters can slow or stop scar-forming cells from thickening the lungs in people with fibrotic lung disease.
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.