How inflammation flips memory killer T cells between protective and harmful roles
Inflammation-driven T Cell Responses and their Dichotomous Effect on Host Immunity
This project looks at how inflammation can turn memory CD8 (killer) T cells into cells that either help clear infections and cancer or cause tissue damage for people with infections, autoimmune diseases, or cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Fred Hutchinson Cancer Center NIH-funded |
| Lab location | 1 site (Seattle, United States) |
| Project ID | NIH-11128808 on NIH RePORTER |
What this research studies
From my perspective as a patient, researchers are comparing two ways memory CD8 T cells get reactivated: by directly recognizing targets (TCR signals) or by inflammation-related chemicals (cytokines). They will study tissue-based immune responses using laboratory models and patient-derived samples to find the signals that switch these cells on and off. The team will measure molecules like granzyme B and interferon-gamma and observe effects on pathogen clearance, tissue damage, and healing. The work aims to pinpoint regulators that could be targeted to stop harmful inflammation while keeping protective immunity intact.
Who could benefit from this research
Good fit: Adults with autoimmune diseases, chronic inflammatory conditions, certain infections, or cancer who are willing to donate blood or tissue samples or attend clinic visits would be the most likely candidates to participate.
Not a fit: People without conditions involving CD8 T cell–driven inflammation or those unwilling to provide samples or travel for visits are unlikely to receive direct benefit from this project.
Why it matters
Potential benefit: If successful, this work could lead to therapies that prevent tissue damage from overactive T cells without undermining the immune system's ability to fight infections or cancer.
How similar studies have performed: Previous research has well described regulation of T cells reactivated through direct receptor signals, but controlling inflammation-driven 'bystander' activation is a newer area with limited prior therapeutic success.
Where this research is happening
Seattle, United States
- Fred Hutchinson Cancer Center — Seattle, United States (Active)
Researchers
- Principal investigator: Prlic, Martin — Fred Hutchinson Cancer Center
- Study coordinator: Prlic, Martin
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.