The Habtezion lab aims to understand immune mechanisms and identify potential immune-based therapeutic targets for pancreatitis and inflammatory bowel disease. Researchers in the lab study leukocyte trafficking and immune responses pertaining to the intestinal tract in states of both health and disease.
Figure 1: Small intestine and colon homing of lymphocytes.
Citation for Fig. 1: Gastroenterology. 2016 Feb;150(2):340-54.
The lab demonstrated a beneficial role and mechanism for heme-oxygenase 1 (HO-1) and its downstream effectors in acute pancreatitis. In chronic pancreatitis the lab characterized macrophage-pancreas stellate cell crosstalk that contributes to disease progression and fibrosis. The significance of this crosstalk is further demonstrated by targeting macrophage polarization and function, as well as altering disease course in established experimental disease. The lab is currently working to elucidate targetable immune pathways that alter and/or reverse the course of disease progression.
Figure 2: Schematic representation of macrophage and pancreatic stellate cell (PSC) interaction in chronic pancreatitis.
Citation for Fig. 2: Nat Commun. 2015 May;6:7158.
Inflammatory bowel disease
A second major project in the lab pertains to understanding immune responses in the intestine and in inflammatory bowel disease (IBD). Multiple projects on intestinal inflammation pertain to understanding the heterogeneity and immune profiles of IBD patients, host immune-microbiome interaction, immune-enteric nervous system interaction, as well as intestine-specific leukocyte recruitment and therapeutic targets using primary clinical samples and experimental models of inflammation. Recently, the lab demonstrated immune signatures consistent with heterogeneous manifestations of IBD and that blood immune signatures can distinguish clinically relevant subsets of IBD and reflect tissue immune responses.
Figure 3. Blood and tissue are immunologically distinct in subsets of inflammatory bowel disease.
Citation for Fig. 3: Nat Commun. 2019 June;10:2686.