Emily Hemann, PhD

About

Biography

Sensing and discrimination of foreign vs host nucleic acids is key for providing protection against pathogens while preventing deleterious inflammation. The retinoic acid inducible gene-I (RIG-I) like receptors (RLRs) are dead-box helicases that detect pathogen-derived nucleic acids, leading to downstream activation of interferon (IFN) and inflammatory pathways for host defense. While progress has been made in describing the distinct ligands that bind to the RLRs contributing to these differential outcomes, we still lack an understanding of the cell-, microenvironment-, and tissue-specific responses downstream of RLRs.

Unravelling these potentially unique mechanisms of RLR and IFN regulation will broaden our knowledge of the function of these critical pathways in tissue homeostasis, pathogenesis, and repair. We utilize novel genetic knockout models of pulmonary inflammation and infection combined with transcriptional and cellular analysis to understand how early innate immune signals program innate and adaptive immunity. Research in the lab focuses on understanding: i) the emerging non-traditional roles of RLRs in regulating disease and tissue repair beyond induction of IFN, and ii) unique cell-intrinsic roles for RLRs and IFN signaling pathways in regulating tissue damage and repair. The ultimate goal of our research is to inform the development of better adjuvants and therapeutics against pulmonary inflammation and viral infection.

Credentials

Research