How dioxin-like chemicals weaken early antibody (IgM) responses by targeting CD5+ innate-like B cells
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
This research looks at whether exposure to dioxin-like chemicals can weaken the body's early antibody (IgM) defense by acting on a specific group of B cells called CD5+ innate-like B cells.
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 ID | NIH-11121927 on NIH RePORTER |
What this research studies
Researchers use human primary B cells and molecular analyses to see how aryl hydrocarbon receptor (AHR) ligands like TCDD change antibody-producing cells. They compare human results with mouse and rat data and use RNA sequencing and protein studies to identify genes and pathways affected, including LCK and PD-1. The team focuses on CD5+ innate-like B cells because these cells produce much of the circulating IgM, especially early and late in life. Findings may include biomarkers of susceptibility and insights into how environmental exposures reduce antibody production.
Who could benefit from this research
Good fit: Ideal participants would be adults willing to provide blood samples, especially those with known or suspected exposure to dioxin-like chemicals or concerns about weakened antibody responses.
Not a fit: People seeking immediate treatment or those without any history of relevant environmental exposure are unlikely to get direct clinical benefit from this laboratory-focused research.
Why it matters
Potential benefit: If successful, this work could identify blood-based markers of susceptibility to dioxin-like exposures and point to ways to protect or monitor immune function in exposed people.
How similar studies have performed: Animal studies and some epidemiological data have shown immune suppression from AHR ligands, but applying those findings to human B-cell mechanisms is relatively new.
Where this research is happening
East Lansing, United States
- 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 below.