IRF7 links immune signals to skin fibrosis in systemic sclerosis
Official title: Interferon Regulatory Factor 7 Links Interferon Pathway Activation to the Exaggerates Fibrotic Response in Systemic Sclerosis
Funded at University of Texas Hlth Sci Ctr Houston · NIH-11325823 · Data updated 2026-11-12
Researchers are testing whether a key immune regulator, IRF7, drives the fibrotic changes seen in systemic sclerosis and whether targeting this pathway could reduce scarring.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Texas Hlth Sci Ctr Houston NIH-funded |
| Lab location | 1 site (Houston, United States) |
| Project start | May 1, 2023 |
| Project end | April 30, 2028 |
| Funding year | 2026 |
| Award (this year) | $278,973 |
| NIH project number | 5R01AR081280-04 |
| Project ID | NIH-11325823 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with systemic sclerosis or related fibrotic conditions who may benefit from future therapies targeting IRF7 pathways.
✕Less likely to help
Patients without systemic sclerosis or those without interferon-related fibrotic activity may not benefit from this approach.
What this research studies
Systemic sclerosis is a serious autoimmune disease where the skin and organs become abnormally fibrotic. This grant focuses on IRF7, a transcription factor in the interferon pathway, to see how it connects immune activation to fibroblast-driven scarring. The team will study IRF7 in dermal fibroblasts, its interaction with TGFβ signaling, and how manipulating IRF7 affects fibrosis in lab models. By combining human-derived cells and mouse models, they aim to clarify a bridge between immune dysregulation and tissue scarring. The ultimate goal is to identify therapeutic strategies that could lessen fibrosis in patients with SSc.
Why it matters
Potential benefit: If successful, this work could reveal a new target to reduce fibrosis and improve outcomes for people with systemic sclerosis.
How similar studies have gone: Previous studies show that modulating IRF7 and interferon signaling can influence fibrosis in experimental models, supporting potential benefit but with translation needed.
Where this research is happening
-
University of Texas Hlth Sci Ctr Houston
Houston, United States Active
Researchers
- Principal investigator: Assassi, Shervin — University of Texas Hlth Sci Ctr Houston
- Study coordinator: Assassi, Shervin
Related research
Other NIH-funded projects on the same topics.
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Understanding how a cell protein (SLC9A1) drives skin and lung scarring in systemic sclerosis
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From proteins and genes to new treatments for scar-related lung disease
A large NIH grant is working to map the proteins in the lungs of people with systemic sclerosis to find new targets for drugs that could slow or stop lung fibrosis.
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Clinical-Translational Studies in Skin, Lung, and Blood Vessel Problems in Systemic Sclerosis
A NIH grant supports coordinated efforts to understand and improve health for people with systemic sclerosis and related conditions by sharing resources, data, and pilot projects at MUSC.
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Role of A20 and DREAM in fat cells and skin scarring in systemic sclerosis
A research project at the University of Michigan looks at how differences in fat tissue and blood vessels relate to skin scarring in systemic sclerosis, with the aim of finding new ways to treat or prevent fibrosis.
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Vasculopathy in Systemic Sclerosis and Lung Disease in Adults
A study in adults with systemic sclerosis will look at how blood vessels in the lungs and body relate to the development of lung disease, with the aim of finding new ways to prevent it.
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.