How sugar-adding enzymes shape immune reactions and diabetes
Official title: Glycosyltransferase Function in Development and Disease
Funded at Sanford Burnham Prebys Medical Discovery Institute · NIH-11393657 · Data updated 2026-11-12
Researchers are looking at how enzymes that add sugars to cell surfaces might change immune attacks on insulin-producing cells in people with or at risk for Type 1 diabetes.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Sanford Burnham Prebys Medical Discovery Institute NIH-funded |
| Lab location | 1 site (La Jolla, United States) |
| Project start | September 15, 1994 |
| Project end | March 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $487,500 |
| NIH project number | 5R01DK048247-29 |
| Project ID | NIH-11393657 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates would be people with Type 1 diabetes, those at high risk (for example, with diabetes-related autoantibodies), or donors willing to provide blood or pancreatic tissue samples.
✕Less likely to help
People with non-autoimmune forms of diabetes (like Type 2) or unrelated conditions are unlikely to benefit directly from this research in the short term.
What this research studies
This project looks at how enzymes called sialyltransferases add sialic acid sugars to proteins on cell surfaces and how those sugars influence immune receptors that control tolerance. Scientists use mouse models, molecular laboratory experiments, and analyses of human pancreatic beta cells or samples to compare how different levels of sialylation affect B cells, autoantibody production, and cell survival. They focus on interactions with Siglec receptors on immune cells that can promote tolerance or permit autoimmune attack. Understanding these steps could point to ways to reduce immune damage to beta cells or identify markers of higher risk for Type 1 diabetes.
Why it matters
Potential benefit: If successful, this work could identify new ways to protect insulin-producing beta cells or prevent autoimmune attacks that cause Type 1 diabetes.
How similar studies have gone: Related animal studies show that changing sialylation or Siglec signaling can reduce lupus-like autoimmunity in mice, but translating these findings to human Type 1 diabetes is still novel and unproven.
Where this research is happening
-
Sanford Burnham Prebys Medical Discovery Institute
La Jolla, United States Active
Researchers
- Principal investigator: Marth, Jamey — Sanford Burnham Prebys Medical Discovery Institute
- Study coordinator: Marth, Jamey
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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.