Dioxin-like chemicals and human B cells: how exposure may weaken antibody defenses
Official title: Project 1 - Dioxin-like Compounds Suppress IgM Responses by Targeting CD5+ (Innate-like) B cells, which can Serve as a Biomarker of Susceptibility to Environmental AHR Ligands
Funded at Michigan State University · NIH-11394777 · Data updated 2026-11-12
Aims to understand how environmental toxins like TCDD can reduce antibody production by a specific human B cell type, potentially making people more vulnerable to infections.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Michigan State University NIH-funded |
| Lab location | 1 site (East Lansing, United States) |
| Project start | April 1, 1997 |
| Project end | June 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $314,444 |
| NIH project number | 5P42ES004911-31 |
| Project ID | NIH-11394777 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with or at risk of exposure to environmental AHR ligands, particularly those with altered B cell function or impaired humoral immunity.
✕Less likely to help
Individuals without exposure to relevant environmental ligands or with non-immune-related health issues may not benefit.
What this research studies
This grant explores how aryl hydrocarbon receptor (AHR) ligands suppress antibody production by human primary B cells, focusing on CD5+ innate-like B cells that contribute early IgM. Researchers will study the molecular pathways, including LCK and PD-1, that may be altered by TCDD exposure and lead to reduced humoral responses. The project uses human B cells and aims to map changes in gene expression and protein signals to explain the observed IgM suppression. Outcomes could identify biomarkers of susceptibility and inform strategies to protect immune function in environmental toxin exposures.
Why it matters
Potential benefit: Understanding these mechanisms could lead to biomarkers for vulnerability and guide interventions to preserve antibody responses in exposed individuals.
How similar studies have gone: Prior work in animals and some human cells suggests AHR ligands can suppress humoral immunity, with human CD5+ B cells showing distinct responses.
Where this research is happening
-
Michigan State University
East Lansing, United States Active
Researchers
- Principal investigator: Kaminski, Norbert E — Michigan State University
- Study coordinator: Kaminski, Norbert E
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.