Humoral immunity and B cell memory are essential components of the adaptive immune response. The goal of my project is to understand the basis of long-term humoral immunity during chronic ehrlichial infection, particularly the generation of B cell memory. To this end, we have focused on a population of CD19+, IgM+ B cells found during chronic ehrlichial infection that express CD11c, a marker typically found on dendritic cell (DC) populations. These CD11c+ IgM memory cells exhibit phenotypic characteristics of memory B cells, including expression of CD73, CD11b, and PD-L2. In addition, these CD11c+ IgM memory cells lack expression of CD138, are largely quiescent, and have accumulated somatic mutations. Although these cells did not proliferate or secrete antibody ex vivo, they produced antigen-specific IgM upon in vitro stimulation with mitogens. Furthermore, in vivo depletion of the CD11c+ IgM memory cells abrogated the IgG recall response to specific antigen challenge. Our findings are consistent with previous data demonstrating that IgM memory cells undergo class switch recombination, and affinity maturation following re encounter with cognate antigen. We propose that these CD11c+ IgM memory B cells are responsible for the IgG produced following secondary challenge in ehrlichial infection, and likely function to provide greater flexibility to variant antigenic challenges. These studies have the potential to impact future vaccine design against bacterial pathogens.

At GE Global Research, I was an individual contributor on multiple global research projects and teams. Our main objective was to develop new molecular imaging agents for the early detection of human disease. These projects included the development of animal models of human disease, and the evaluation of novel imaging agents using these models.

As a research technician in a large laboratory, I participated in the development of cancer cDNA and shRNA libraries. I was responsible for the maintenance of various cell lines, and performed experiments as required. I also received training in flow cytometry, and was responsible for sorting stably transfected cell lines on their expression of the reporter green fluorescent protein (GFP). During a transition period between core directors, I was responsible for managing and maintaining the flow cytometry core for the Ordway Research Center.

As a research technician, I was responsible for managing and maintaining the laboratory. My duties included animal husbandry, ordering, and general lab maintenance. My specific research project was to create CD4+ T cell hybridomas specific for the early secretory antigenic target-6 (ESAT-6) of Mycobacterium tuberculosis. The T cell receptor from this T cell clone was used to create a transgenic mouse for following antigen-specific T cell responses during Mycobacterium tuberculosis infection. Other projects included antigen-specific T cell stimulation assays on Mycobacterium tuberculosis infected tissue under BSL-3 conditions.