How allergic inflammation may weaken skin immune cells that fight viruses
Effect of Th2-type microenvironment on CD8 TRM-mediated protection from infection
This project looks at whether allergic-type inflammation stops skin memory T cells from protecting adults with atopic dermatitis against viral infections.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Massachusetts General Hospital NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project ID | NIH-11324533 on NIH RePORTER |
What this research studies
Researchers will examine why people with atopic dermatitis have more severe or recurring skin viral infections by focusing on tissue-resident CD8+ memory T cells (TRM) that normally defend the skin. They will use mouse models of allergic eczema to see if Th2-type inflammation and IL-4 reduce TRM persistence and increase susceptibility to herpes simplex virus. The team will also study human skin CD8+ TRM and expose them to Th2 cytokines to observe changes in their function and survival. Finally, they will analyze how IL-4 alters TGF-β receptor signaling and the chromatin landscape of CD8+ T cells using methods such as ATAC-seq to identify molecular mechanisms behind TRM loss.
Who could benefit from this research
Good fit: Adults (21+) with atopic dermatitis or allergic eczema, especially those with a history of recurrent or severe skin viral infections, would be the most relevant candidates for the human-sample parts of this research.
Not a fit: People without atopic dermatitis or whose infections stem from broader systemic immunodeficiencies are unlikely to receive direct benefit from this specific line of work.
Why it matters
Potential benefit: If successful, this work could point to ways to restore or protect skin immune memory and reduce serious viral infections in people with atopic dermatitis.
How similar studies have performed: Previous studies show TRM protect against skin infections and Th2 signals change immune behavior, but linking IL-4–driven chromatin changes to TRM loss in atopic dermatitis is a newer and less-tested idea.
Where this research is happening
Boston, United States
- Massachusetts General Hospital — Boston, United States (Active)
Researchers
- Principal investigator: Bromley, Shannon K — Massachusetts General Hospital
- Study coordinator: Bromley, Shannon K
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.