Tiffany Horng

Tiffany Horng

Associate Professor of Genetics and Complex Diseases

Department of Genetics and Complex Diseases
Department of Immunology and Infectious Diseases

655 Huntington Avenue
Building 2, 1st Floor
Boston, Massachusetts 02115


Ph.D., 2003, Yale University
B.A., 1999, UC Berkeley

Other Affiliations

Ph.D. Program in Biological Sciences in Public Health


The lab is broadly interested in macrophage biology in the context of innate immunity and inflammation. Macrophages are pleiotropic cells that assume a variety of functions depending on their tissue of residence and tissue state. Such functional specialization requires appropriate macrophage activation or polarization, triggered by a variety of factors including microbial products and cytokines. One focus of the lab is in elucidating the metabolic underpinnings of macrophage activation. In particular, we are interested in how macrophage polarizing signals co-opt metabolic signaling pathways to coordinate macrophage activation and metabolism, and how perturbation of this process in pathophysiological contexts like chronic nutrient excess impairs macrophage activation and disease progression. In general, dysregulated macrophage activities contribute to many diseases, including infectious, inflammatory, and metabolic diseases and cancer, thus a better understanding of metabolic control of macrophage activation could pave the way to the development of new therapeutic strategies.

A related focus of the lab is on the NLRP3 inflammasome pathway. The NLRP3 inflammasome is a cytosolic complex that that activates the proinflammatory caspase, Caspase-1, thus promoting maturation and release of IL-1b and IL-18. As such the NLRP3 inflammasome plays a critical role in many physiological and pathophysiological settings, including host defense as well as chronic inflammatory diseases like obesity and type 2 diabetes. How the NLRP3 inflammasome is activated in these contexts is not well understood, and in ongoing studies we seek to uncover how cellular metabolism modulates NLRP3 inflammasome activation.