Research Interests and Projects


  • Immunology of parasitic helminth infection

    • Type 2 inflammation 

    • Mucosal epithelia

    • Macrophage subsets

  • Immunology of mucosal injury and repair

    • Epithelial restitution

    • Fibrosis

    • Wound healing cascade


“Alternative macrophage activation limits immunopathology”

Alternatively activated macrophages (M2 cells) are important for the regulation of tissue injury and inflammation caused by certain worm infections (Herbert et al. Immunity 2004).  Arginase I, a catabolic enzyme of L-arginine, is highly up-regulated in M2 cells and may serve to suppress inflammation through direct or indirect mechanisms. This project uses several myeloid-specific gene targeted mice to investigate whether Arginase I and TGF-beta are necessary for the regulation of mucosal Type 2 inflammation.

“Trefoil factors regulate Type 2 immunity”

Trefoil factor 2 (a mucus-stabilizing protein that drives epithelial cell restitution) is rapidly induced within the lung following N. brasiliensis infection and controls IL-33 production within epithelial cells, macrophages and inflammatory DC (Wills-Karp 2012). This is particularly exciting, given the intense debate centered upon the initiation and regulation of Type 2 immunity.  This project will utilize conditional gene deletion in mice to further characterize the importance of TFF family members in the cell-specific regulation of Type 2 cytokines and mucosal macrophage function.  We possess several novel model systems to investigate these areas.

Pilot studies

Trefoil factors regulate mucosal Type 1 inflammation

Orchestration of pro-inflammatory and anti-inflammatory responses is critical for the clearance microbial infection and avoidance of lethal immunopathology. Given the essential role of Trefoil factor proteins in restitution, this project investigates whether Trefoils suppress TH1/TH17-associated inflammation in addition to promoting wound healing. Indeed, mice lacking TFF2 show enhanced homeostatic inflammation and Type 1 immunity against oral infection with the human microbial pathogen Toxoplasma gondii  (McBerry et al. Journal of Immunology 2012.)

TGF-beta regulates mucosal myeloid cell function

Transforming growth factor beta is a well-established regulator of inflammation and tissue remodeling, but whether tissue macrophages require TGF-beta responsiveness to promote homeostasis, immunity, or extra-cellular matrix turnover remains unknown. We possess mice that lack TGF-beta responsiveness macrophages and neutrophils or dendritic cells to address these issues.