How metabolism helps remove self‑reactive (anti‑DNA) B cells while preserving protective antibody‑making B cells
Metabolic enforcement of selection in anti-DNA B cells vs. antigen-specific B cells
This project looks at how metabolic signals decide whether B cells that target your own DNA are killed or whether helpful antibody‑making B cells survive, which is important for autoimmune diseases like lupus.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Florida NIH-funded |
| Lab location | 1 site (Gainesville, United States) |
| Project ID | NIH-11171695 on NIH RePORTER |
What this research studies
Researchers are studying why B cells that react to the body's own DNA are usually removed while B cells that fight infections are expanded. They focus on metabolic pathways—especially mTORC1 signaling, mitochondrial oxidative phosphorylation, and the ubiquitin ligase Itch—that influence whether a B cell survives or undergoes apoptosis. The team uses laboratory cellular and animal models and molecular experiments to compare autoreactive versus antigen‑specific B cells, and may use human‑relevant samples to link findings to autoimmune disease. Understanding these differences could point to ways to selectively target harmful B cells without weakening normal immune responses.
Who could benefit from this research
Good fit: People with antibody‑driven autoimmune diseases—particularly systemic lupus erythematosus or other conditions with anti‑DNA autoantibodies—would be most relevant to provide samples or join related future trials.
Not a fit: Patients whose illnesses are not driven by autoantibodies or who have non‑immune causes of disease are unlikely to get direct benefit from this work.
Why it matters
Potential benefit: If successful, this work could lead to therapies that selectively eliminate self‑reactive B cells and reduce autoimmune inflammation with fewer side effects than broad immunosuppression.
How similar studies have performed: Previous studies have linked metabolism and mTOR signaling to B cell survival, but using Itch‑dependent metabolic control to selectively remove autoreactive B cells is a relatively new, mainly preclinical approach.
Where this research is happening
Gainesville, United States
- University of Florida — Gainesville, United States (Active)
Researchers
- Principal investigator: Moser, Emily K. — University of Florida
- Study coordinator: Moser, Emily 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.