Jeremy Mogridge, PhD

Associate Professor

To initiate a protective response to an infection, mammals must detect microbial pathogens directly or detect the damage that they cause.  The immune sensor that we are studying detects the presence of microbial pathogens by monitoring the alterations in cellular metabolism caused by intracellular bacteria.  This sensor, called NLRP1B, becomes activated in cells undergoing energy stress. Activated NLRP1B forms an inflammasome complex that processes pro-caspase-1 to generate an immune response.  We are interested in understanding the molecular mechanisms behind these events.

Selected Publications:

  1. Neiman-Zenevich J, Stuart S, Abdel-Nour M, Girardin SE, Mogridge J. Listeria monocytogenes and Shigella flexneri Activate the NLRP1B Inflammasome. Infect Immun. 2017 Oct 18;85(11). pii: e00338-17.
  2. Neiman-Zenevich J, Liao KC, Mogridge J. Distinct regions of NLRP1B are required to respond to anthrax lethal toxin and metabolic inhibition. Infect Immun. 2014 Sep;82(9):3697-703
  3. Frew BC, Joag VR, Mogridge J. Proteolytic processing of Nlrp1b is required for inflammasome activity. PLoS Pathog. 2012;8(4):e1002659.