How a pollutant‑sensing protein (AhR) changes immune-driven inflammation
The impact of Aryl hydrocarbon receptor signaling on Toll like receptor-mediated inflammation
This research looks at how a protein that senses environmental chemicals can change immune reactions linked to asthma and autoimmune diseases.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California at Davis NIH-funded |
| Lab location | 1 site (Davis, United States) |
| Project ID | NIH-11234289 on NIH RePORTER |
What this research studies
Researchers will use lab studies and mouse models to see how the aryl hydrocarbon receptor (AhR) and its repressor (AhRR) alter communication between antigen‑presenting dendritic cells and T cells. They will focus on how AhR signaling interacts with Toll‑like receptor and NF‑kB pathways after exposure to AhR‑activating chemicals such as dioxins. The team uses transgenic mice that overexpress AhRR, molecular analyses of inflammatory gene expression, and cell‑level experiments to trace these signaling changes. Results are intended to clarify how environmental exposures may trigger or worsen autoimmune and allergic immune responses.
Who could benefit from this research
Good fit: Although the project is lab‑based, people with autoimmune diseases, inflammatory conditions, or asthma — or those with known exposure to environmental pollutants — are the patient groups most likely to benefit from the findings.
Not a fit: People without immune‑driven conditions or without relevant environmental exposures are less likely to see direct benefit from this specific basic science work.
Why it matters
Potential benefit: If successful, this work could reveal mechanisms linking environmental toxins to autoimmune and allergic diseases and point to new prevention strategies or drug targets.
How similar studies have performed: Prior studies have shown AhR affects T cell differentiation and immune responses, but the specific role of AhRR and its interaction with TLR/NF‑kB signaling is less well understood.
Where this research is happening
Davis, United States
- University of California at Davis — Davis, United States (Active)
Researchers
- Principal investigator: Vogel, Christoph F a — University of California at Davis
- Study coordinator: Vogel, Christoph F a
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.