Martin Alexander Kriegel MD/PhD
Assistant Professor of Immunobiology and of Medicine (Rheumatology); Assistant Professor of Medicine (Rheumatology)
Microbiome; commensals; lymphocytes; autoimmunity; Th17 cells; antiphospholipid syndrome; beta2-glycoprotein; lupus; type 1 diabetes
The gut microbiota, the collection of trillions of commensals colonizing the gastrointestinal tract, does not elicit a pathologic immune response in healthy hosts even though immune cells are constantly in contact with microbial antigens at the mucosal surfaces. This phenomenon is partly due to the fact that the human gut microbiota and immune system have co-evolved for millennia with the host. Diet and environmental influences that have shaped these processes in the past are very different in today’s societies. Recent changes in the gut microbial community composition are thought to contribute to metabolic and immune-mediated diseases. An emerging theme in autoimmunity research is that outgrowth of detrimental commensals (“pathobionts”) or loss of beneficial commensals (“symbionts”) unleashes the autoimmune process in a genetically susceptible host by various mechanisms. While evidence exists for this paradigm in some mouse models, the proof in human autoimmune diseases is still outstanding. A major aim of this laboratory is to characterize the gastrointestinal microbiome of both mice and humans with systemic autoimmune diseases, and to potentially prove causal relations with humanized gnotobiotic animals. The ultimate goal is to develop novel biomarkers and therapeutic strategies for human autoimmune diseases.