B cells that make abnormal IgA1 in IgA kidney disease
Official title: Distinct Glycophenotypes with Abnormal Signaling Define a Subpopulation of B cells Responsible for Production of Galactose-Deficient IgA1, the Main Autoantigen in IgA Nephropathy
Funded at University of Alabama at Birmingham · NIH-11235941 · Data updated 2026-11-12
Researchers are identifying a group of B cells that produce a harmful form of IgA1 in people with IgA nephropathy to help guide future treatments.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Alabama at Birmingham NIH-funded |
| Lab location | 1 site (Birmingham, United States) |
| Project start | February 15, 2023 |
| Project end | November 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $497,782 |
| NIH project number | 5R01DK134489-04 |
| Project ID | NIH-11235941 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with biopsy-confirmed IgA nephropathy or elevated galactose-deficient IgA1 levels would be the most relevant candidates for sample donation or related participation.
✕Less likely to help
Individuals without IgA nephropathy or with other unrelated kidney diseases are unlikely to receive direct benefit from this project.
What this research studies
This project looks for the specific B cells that make galactose-deficient IgA1, the abnormal antibody linked to kidney damage in IgA nephropathy. Using patient blood and biopsy-derived samples, the team will isolate B cells and apply molecular techniques, including ATAC-seq and signaling assays, to compare cell identity and activity in patients versus healthy donors. They will examine how these B cells are regulated and how they generate the galactose-deficient IgA1 form, using both primary and immortalized patient-derived cells in the lab. The aim is to identify molecular markers and signaling pathways that could become targets for therapies or tests to predict disease progression.
Why it matters
Potential benefit: If successful, this work could enable targeted treatments or diagnostics that prevent formation of harmful IgA complexes and slow kidney damage in IgA nephropathy.
How similar studies have gone: Prior laboratory studies have shown that B cells from IgA nephropathy patients produce more galactose-deficient IgA1, but translating those findings into targeted therapies is still early and largely untested.
Where this research is happening
-
University of Alabama at Birmingham
Birmingham, United States Active
Researchers
- Principal investigator: Reily, Colin Robert — University of Alabama at Birmingham
- Study coordinator: Reily, Colin Robert
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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.