Biography and Expertise
Decoding the microbiome to restore immune balance and transform care in multiple sclerosis, cancer, and chronic inflammatory disease.
We humans have evolved as holobionts, organisms whose biology is shaped not only by our own genome but also by the microbial communities (microbiome) that live within and on us. These microbes play essential roles in human physiology, including educating the immune system and maintaining the balance between tolerance and inflammation. Using a bedside-to-bench-to-bedside approach, we integrate human microbiome profiling with mechanistic studies in immune cells, organoids, and animal models to define how microbial communities and their metabolites shape immune function, mucosal homeostasis, and host responses in health and disease.
Most commensal microbes act as beneficial symbionts ("good" bugs), supporting immune training, barrier integrity, and metabolic balance. Key symbionts such as Prevotella and Bifidobacterium are consistently depleted in inflammatory diseases, particularly multiple sclerosis (MS), where their loss is associated with impaired immune regulation. Microbes, however, are not inherently fixed as good or bad: a commensal organism can shift into a pathogenic state ("bad" bug, or pathobiont) when its local environment changes. Inflammation itself accelerates this shift, creating ecological pressure that depletes symbionts and enriches pathobionts, fueling a self-reinforcing cycle of immune activation. A striking example is Akkermansia muciniphila, often beneficial in metabolic health but enriched in MS, where it is associated with Th1/Th17-driven neuroinflammation. Diet, cytokine milieu, HLA genetics, hormones, infections, and environmental exposures all influence these good-to-bad functional switches. Defining the drivers of this microbial imbalance, and developing strategies to restore symbionts while limiting pathobionts, is central to rebuilding immune homeostasis.
Our laboratory investigates how these context-dependent microbiome-immune interactions shape diseases such as MS. We also study how HLA class II polymorphisms (the strongest genetic risk factor for MS), diet, sex hormones, and environmental exposures reshape microbial communities toward tolerance or chronic inflammation. We extend these principles to cancer immunobiology and to understanding how environmental toxicants disrupt the microbiome to alter immune homeostasis.
Research Interests
- Human commensals as therapeutic agents
- Gut microbiome–immune interactions
- Cellular and cytokine-mediated immune responses
- Inflammation and immune regulation
- HLA genetics and transgenic mouse models
- Multiple sclerosis and other autoimmune diseases
- Neurological diseases
- Cancer immunobiology
- Environmental exposures and immune homeostasis
Keywords
Multiple sclerosis, neurological diseases, EAE, MHC/HLA transgenic mice, gut microbiome, cytokines, human commensals as therapeutics, autoimmune disease, cancer immunobiology