How donor HLA antibodies trigger blood-vessel injury after transplant
Official title: The role of HLA and its coreceptors in endothelial cell activation and leukocyte recruitment in antibody-mediated transplant rejection
Funded at University of California Los Angeles · NIH-11258860 · Data updated 2026-11-12
Learning how antibodies against donor HLA make the graft's blood vessels activate and draw in immune cells in transplant patients.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California Los Angeles NIH-funded |
| Lab location | 1 site (Los Angeles, United States) |
| Project start | September 1, 2018 |
| Project end | January 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $733,806 |
| NIH project number | 5R01AI135201-08 |
| Project ID | NIH-11258860 on NIH RePORTER |
Who could benefit from this research
✓Could help
Solid-organ transplant recipients who have donor-specific HLA antibodies (DSA), especially those at risk for chronic antibody-mediated rejection such as heart transplant patients, would be ideal candidates.
✕Less likely to help
People without donor-specific antibodies or whose rejection is driven primarily by T-cell mechanisms rather than antibodies may not benefit directly from this work.
What this research studies
As a transplant patient, this work looks at how antibodies that target donor HLA cause the lining of blood vessels in my graft to change and attract white blood cells. Researchers will study endothelial cells in the lab, examine interactions between HLA and co-receptors such as TLR4 and integrin β4, and analyze samples from transplant patients to trace the signaling steps. They will measure things like Weibel-Palade body release and P-selectin exposure and test how blocking specific pathways changes monocyte recruitment. The aim is to pinpoint molecular targets that could prevent transplant vasculopathy and chronic antibody-mediated rejection.
Why it matters
Potential benefit: Could identify new targets or treatments to prevent chronic antibody-mediated rejection and help transplanted organs last longer.
How similar studies have gone: Prior studies have linked HLA antibodies and TLR4-related signaling to endothelial activation, but translating those findings into proven therapies remains largely untested.
Where this research is happening
-
University of California Los Angeles
Los Angeles, United States Active
Researchers
- Principal investigator: Reed, Elaine F — University of California Los Angeles
- Study coordinator: Reed, Elaine F
Related research
Other NIH-funded projects on the same topics.
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Using blood biomarkers to guide immunosuppression after liver transplant
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Targeting YAP and TAZ with statins to prevent transplant rejection from donor antibodies
A study to see if statins can block specific gene regulators (YAP and TAZ) to protect transplanted organs from rejection caused by donor antibodies.
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Predicting acute rejection in children after heart transplant
A study to improve how doctors predict if a child who has had a heart transplant will have acute rejection using noninvasive blood markers and advanced heart MRI analysis.
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.