The exhibits
Decoding the CD4 T cell
Three rooms. One cell type — the conductor of adaptive immunity — studied from its birth as a lineage, through its life in the tissue, to its part in disease.
Room I — Foundations
Th17 cells and the logic of T-helper differentiation
For two decades, effector CD4 T cells came in two kinds. In 2005, work from this lab described a third — the Th17 lineage — and with it a new account of how the immune system organizes inflammation and host defense.
The study continues. We dissect the transcriptional and metabolic circuitry that commits a naive T cell to the Th17 fate, the signals that hold that program stable or let it convert to other states, and how Th17 cells coordinate defense at barrier surfaces.
Room II — Tissue
Mucosal and intestinal immunity
The intestine is the body's largest immune organ and a constant negotiation between tolerance and defense. We study how effector and effector-regulatory (eTreg) CD4 T cells develop in the gut, and how nuclear receptors and the microbiota shape their behavior.
With reporter mice, fate-mapping, and single-cell methods, we follow individual T cells through differentiation in their native tissue — asking not just what a cell is, but how it got there and what it does next.
Room III — Disease
When T-cell programs go wrong
The pathways that defend the gut can also drive disease. Our work spans inflammatory bowel disease, the passage from chronic inflammation to colorectal cancer, and the mechanisms controlling late-onset sepsis in neonates.
By understanding how protective responses tip into pathology, we look for the points where they might be safely redirected — the foundation for more precise immunotherapies.
The vitrine
Materials & methods
Genetic reporter and fate-mapping mouse models · single-cell transcriptomics · in vivo models of mucosal infection and inflammation · cytokine and nuclear-receptor signaling · primary human tissue collaborations across UAB.