Genetic clues about dangerous colitis-causing T cells
Official title: Genetic variants guiding pathogenicity of colitogenic T cells
Funded at Benaroya Research Inst at Virginia Mason · NIH-11364994 · Data updated 2026-11-12
This grant looks at how genetic differences in people with inflammatory bowel disease influence the behavior of disease-causing T cells called Th17 cells.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Benaroya Research Inst at Virginia Mason NIH-funded |
| Lab location | 1 site (Seattle, United States) |
| Project start | September 1, 2024 |
| Project end | June 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $509,200 |
| NIH project number | 5R01DK140972-03 |
| Project ID | NIH-11364994 on NIH RePORTER |
Who could benefit from this research
✓Could help
Individuals with inflammatory bowel disease whose genetic variants are being studied through blood samples and related analyses.
✕Less likely to help
People without IBD or who do not carry the studied genetic variants may see little direct benefit.
What this research studies
Researchers will study how non-coding genetic variants in people with IBD change the activity of regulatory DNA in Th17 cells, which may make these cells more inflammatory. They will use a method called massively parallel reporter assays to test allele-specific effects on gene regulation. The work focuses on linking genetic variation to changes in Th17 cell function that could drive colitis. Findings could point to specific genetic factors that worsen disease and guide new treatment approaches. This project involves human data and blood-derived cells to understand disease biology.
Why it matters
Potential benefit: Understanding genetic drivers of Th17 cell pathogenicity could lead to more precise therapies for IBD.
How similar studies have gone: Prior work has shown that regulatory genetic variants can affect immune cell function, supporting this approach.
Where this research is happening
-
Benaroya Research Inst at Virginia Mason
Seattle, United States Active
Researchers
- Principal investigator: Ray, John Philip — Benaroya Research Inst at Virginia Mason
- Study coordinator: Ray, John Philip
Related research
Other NIH-funded projects on the same topics.
-
T cells and the switch from pre-autoimmunity to autoimmune disease
A study following people at risk for type 1 diabetes and people with Down syndrome to understand how certain T cells may shift toward causing autoimmune disease.
-
Genetic and epigenetic control of T cell function in autoimmune disease
This grant aims to understand how genetic and epigenetic changes affect how T cells behave in autoimmune diseases to find ways to reduce harmful immune responses.
-
Immune Tolerance Network (ITN) for immune tolerance therapies across autoimmune and allergic diseases
A national network runs clinical trials to test new immune-tolerance therapies that could help people with autoimmune and allergic diseases.
-
Immune Tolerance Network for safer, more effective immune therapies
A nationwide network tests new immune therapies to help people with autoimmune diseases, allergies, and transplant patients reach better control of their immune system.
-
Immune tolerance research network for safer transplant and autoimmune therapies
A national effort tests new treatments that make the immune system tolerate transplanted organs and fight autoimmune and allergic diseases more safely.
-
Immune Tolerance Network for allergy, autoimmunity, and transplantation
A large NIH program tests new immune-tolerance therapies to help people with autoimmune diseases, allergies, and transplant patients.
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.