Our lab studies how immune responses are regulated within injured and infected tissues. We work at the intersection of immunology, structural biology, and microbiology to gain fundamental insights into disease pathogenesis and to develop novel therapeutics. Major current areas of investigation include:
Bacteriophage / Immune Interactions
We have identified novel roles for bacteriophage in the pathogenesis of infections caused by the bacterial pathogen Pseudomonas aeruginosa. We recently reported that Pf phage produced by P. aeruginosa are internalized by human cells at sites of infection and trigger maladaptive anti-viral immune responses that suppress clearance of bacterial infections. Further, a vaccine that targets these phage prevents the establishment of chronic wound infections (DOI: 10.1126/science.aat9691). Together with the Secor Lab at the University of Montana, we reported that Pf phage act as structural elements in microbial biofilms (doi: 10.1016/j.chom.2015.10.013) and promote bacterial phenotypes associated with chronic infections (DOI: 10.1128/IAI.00648-16) and DOI: 10.1126/scitranslmed.aau9748). Current efforts are focused on understanding how bacteriophage influence mammalian immunity (DOI:10.3390/v11010010) and clinical outcomes in diabetic wound infections.
Diabetic Wound Infections
Chronic wounds are sites of immune dysregulation and interplay between host and microbial factors. We use models of diabetic wound healing to study how tissue inflammation, particularly the extracellular matrix, governs wound healing and local immune defense. Current investigations are focused on studying how hyaluronan and other ECM components influence wound healing, the bioactivity of local cytokines and chemokines, and leukocyte metabolism.
Immune Regulation in Diabetes
We are interested in how immune dysregulation occurs in diabetes. We focus on the extracellular matrix polymer hyaluronan and its influence on the number and function of regulatory T-cells in autoimmune, Type 1 diabetes (T1D). We have previously reported that the extracellular matrix contributes to the progression of autoimmune insulitis (DOI: 10.1172/JCI79271, DOI: 10.2337/db13-1658) and other autoimmune diseases (DOI: 10.1073/pnas.1525086113). Current efforts are focused on understanding how the ECM influences antigen presentation, cytolytic killing, and cellular metabolism.
Interested in joining the lab?
We take high school and undergraduate students through the SSRP program: https://biosciences.stanford.edu/prospective/diversity/ssrp/
For Stanford Undergraduates interested in joining the lab, we require a minimum commitment of a full year (including full-time work in the lab for at least one summer). If you are interested, please contact Dr. Bollyky at firstname.lastname@example.org.