In order to induce a pathogen-neutralizing immune response, DC must be able to function even when confronted with pathogens that have evolved subversive mechanisms.
My interest is in understanding the detailed interactions between DC and bacterial and viral pathogens, that promote DC maturation, and by extension, the development of an effective immune response.
My studies utilize two model pathogens, Listeria monocytogenes, a Gram-positive facultative intracellular bacterium, and Vesicular Stomatitis Virus (VSV), a prototypic negative strand RNA virus, to address this question.
Both Listeria monocytogenes and VSV have developed strategies that allow them to grow and spread within DC populations. Our projects include:
Understanding how DC mature when infected with w.t. VSV
This virus produces a protein (“M”) that effectively shuts down host gene expression and protein production in a wide range of cell types. One specific type of in vitro-propagated DC, representative of resident splenic populations in mice, is able to mature even in the presence of M protein. The molecular events that allow for DC maturation under these circumstances is one topic of study.