The Flamio Lab studies how vertebrate immune systems detect microbial proteins and how these recognition systems are encoded and regulated in the genome. We focus on fundamental mechanisms governing microbial sensing, receptor evolution, and innate immune signaling across vertebrates.

We use comparative genomics and transcriptomics to define how microbial sensing pathways evolve and how gene regulatory architecture, including untranslated regions (UTRs), microRNAs, and other noncoding elements, controls receptor expression and downstream signaling programs. Our goal is to identify general principles governing how immune receptor systems are constrained, diversified, and functionally tuned over evolutionary time.

Current work uses Toll-like receptor signaling pathways, including Toll-like receptor 5 (TLR5), as model systems to study how conserved microbial recognition receptors evolve and how their genomic and transcriptional regulation shapes immune signaling output.

We analyze immune transcriptomic variation in inflammatory diseases including Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA) to investigate how conserved innate immune signaling programs are reorganized across heterogeneous disease-associated immune states and patient subsets.

Across these systems, our goal is to define the evolutionary and regulatory principles that govern microbial sensing systems and host–microbe interactions, generating diversity in immune responses across vertebrates and human disease. We train students in computational biology, comparative immunogenomics, and transcriptomic analysis, with an emphasis on reproducible, quantitative approaches to host–microbe systems biology and microbial genomics.