Targeting IgSF11 to prevent inflammatory bone loss
IgSF11 Signaling Controls Osteoclast Maturation and Pathogenic Bone Loss
This work looks at whether blocking a cell-surface protein called IgSF11 and its effects on cell metabolism can help people with inflammatory bone loss such as that seen in arthritis.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Pennsylvania NIH-funded |
| Lab location | 1 site (Philadelphia, United States) |
| Project ID | NIH-11232311 on NIH RePORTER |
What this research studies
From a patient perspective, the team is studying how a protein on bone-resorbing cells (osteoclasts) called IgSF11 drives those cells to over-mature and cause bone loss during inflammation. They used laboratory methods including mass spectrometry to find that IgSF11 affects a metabolic enzyme (PKM2) and will test how that pathway controls bone damage. In mice lacking IgSF11 and in an inflammation-driven bone-loss model (LPS), investigators will examine whether blocking IgSF11–PKM2 signaling prevents bone erosion while preserving normal bone formation. They will also try small-molecule approaches that modify PKM2 activity to see if this reduces inflammatory bone loss without blocking the bone-building side of the process.
Who could benefit from this research
Good fit: People with inflammatory bone loss conditions (for example rheumatoid arthritis or inflammation-related bone loss) who are concerned about bone erosion could be the eventual candidates for therapies developed from this work.
Not a fit: Patients whose bone loss is driven primarily by hormonal or age-related osteoporosis, genetic bone disorders, or non-inflammatory causes may not benefit from an IgSF11/PKM2-directed approach.
Why it matters
Potential benefit: If successful, this approach could lead to treatments that prevent inflammatory bone erosion while keeping bone formation intact, reducing joint damage in conditions like inflammatory arthritis.
How similar studies have performed: Existing treatments that reduce osteoclast numbers (like bisphosphonates or RANKL inhibitors) work to limit bone loss but can impair bone formation, and targeting osteoclast maturation or metabolism (IgSF11/PKM2) is a newer, mostly preclinical strategy with promising animal data but limited human testing so far.
Where this research is happening
Philadelphia, United States
- University of Pennsylvania — Philadelphia, United States (Active)
Researchers
- Principal investigator: Choi, Yongwon — University of Pennsylvania
- Study coordinator: Choi, Yongwon
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.