Three modules, one cell type.

M.01 / Foundations

Th17 cells and the logic of T-helper differentiation

In 2005 this lab reported a third lineage of effector CD4 T cells — Th17 — distinct from the Th1 and Th2 paradigms that had defined the field for two decades. That single observation reframed how immunologists think about inflammation and host defense.

The question now is mechanism: which transcriptional and metabolic circuits commit a naive T cell to the Th17 fate, what keeps the program stable or lets it convert to other states, and how Th17 cells coordinate defense at barrier surfaces. In the atlas on the front page, color by Il17a or Il22 at day 14 to watch the program at work.

→ Fig. 01 preset: Il17a at d14

M.02 / 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 tune their behavior.

One current line of work asks whether the gut lining itself instructs T cells: deleting MHC-II from intestinal epithelial cells alone (H2-Ab1 ΔIEC) and profiling 558,304 cells across a Citrobacter rodentium infection — epithelium, intraepithelial lymphocytes, and lamina propria, days 0 to 42. That experiment is the atlas on the front page.

→ Fig. 01 preset: the knockout goes dark

M.03 / Disease

When T-cell programs go wrong

The same pathways that defend the gut drive disease when dysregulated. Our work spans inflammatory bowel disease, the transition from chronic inflammation to colorectal cancer, and the mechanisms controlling late-onset sepsis in neonates.

By measuring how protective responses tip into pathology — at the resolution of single cells and single time points — we aim to find where they can be safely redirected: the foundation for more precise immunotherapy.