Cathryn Nagler graduated with honors from Barnard College, Columbia University. She obtained her PhD from the New York University Grossman School of Medicine and did a postdoctoral fellowship at the Massachusetts Institute of Technology. She was Associate Professor of Pediatrics (Immunology) at Harvard Medical School prior to joining the University of Chicago in 2009.
Nagler serves in national and international leadership roles, many of which are related to publication and teaching, for the American Association of Immunologists, the Society for Mucosal Immunology and Federation of Clinical Immunology Societies. She also participates in numerous review panels.
Nagler received the Distinguished Faculty Award for Leadership in Program Innovation from the University of Chicago in 2017. She was listed among Crain’s Chicago Business Tech Top 50 Women in 2018 and Notable Women in HealthCare in 2019 for her work with her academic start-up company ClostraBio. Academic honors include the American Academy of Allergy, Asthma and Immunology (AAAAI) Foundation and Louis M. Mendelson Award Lectureship and the Siegel Lectureship at the University of California, Los Angeles. She was elected as a Distinguished Fellow of the American Association of Immunologists (AAI) in 2020. She was recently named AAI Program Chair and, as such, is an ex officio member of the AAI Leadership Council.
Nagler Lab studies the mechanisms governing tolerance to dietary antigens. They were one of the first to identify a link between resident intestinal bacteria and the regulation of mucosal immunity. During the last fifteen years, their work has focused on examining how commensal bacteria regulate susceptibility to allergic responses to food. They have proposed that the striking generational increase in food allergies can be explained, in part, by alterations in the composition and function of the commensal microbiome.
In support of this hypothesis, Nagler Lab described a role for a particular population of mucosa-associated commensal bacteria in protection from allergic sensitization in mice. Initial translational studies showed that the composition of the fecal microbiota is altered in infants with cow’s milk allergy. To understand how the microbiota regulates allergic disease in humans they have colonized germ free mice with human bacteria from the feces of healthy or cow’s milk allergic (CMA) infants.
The group discovered that mice colonized with CMA infants’ microbiota exhibited an anaphylactic response to the cow’s milk allergen b-lactoglobulin, while mice colonized with healthy infants’ microbiota were protected against an allergic response. They defined a microbiota signature that distinguishes the CMA and healthy populations in both the human donors and the colonized mice. Analysis of gene expression in ileal intestinal epithelial cells of colonized mice identified a significant correlation between the genes associated with allergy protection and taxa from the Lachnospiraceae family, supporting a causal role for specific bacterial species in protection against food allergy.
These robust, pre-clinical, gnotobiotic models are an ideal system to identify key host-microbial interactions that contribute to allergic sensitization to food. With support from the Polsky Center for Entrepreneurship and Innovation, Nagler Lab has created a start-up company, ClostraBio, to develop novel microbiome-modulating therapeutics to prevent or treat food allergy.