Experience

University of Colorado Anschutz Medical Campus

• United States
• Higher Education
• 700 & Above Employee

• Post Doc Fellow

  • Jul 2017 - Present

  Currently, as a post-doc in Dr. Janoff’s lab, I am building on my experience with both T regulatory cells and regulation of AID in mice. The current project involves characterization of the mechanisms of T cell help for B cell differentiation in response to polysaccharide vaccines during HIV infection. The work provides the opportunity and the challenge to characterize phenotypic and functional outcomes of T and B cells in response to polysaccharides (with and without protein conjugates) in humans in vivo. I am developing more reductionist models of interacting purified T and B cell populations from these HIV-infected and control subjects to explain mechanisms underlying the clinical phenotypes. This work advances both the breadth and the depth of my immunologic expertise for a career. Studying the population dynamics of T follicular helper cells and T follicular regulatory cells driving antigen-specific B cell responses. This project provides a robust opportunity to expand my knowledge in human immunology and to create instructive models of human immune responses with complementary mouse models as needed. This work with humans and HIV can provide a technical and intellectual platform for future work of international importance, such as with tuberculosis.



The University of Pennsylvania

• Post Doc

  • Nov 2011 - Jun 2014

  I investigated the functions of transcription factor YY1 in formation of germinal centers. I designed yy1flox/flox, γ1 CRE mice in which yy1 is deleted once B cells are activated to class switch and express IgG1 antibody. These mice were used to study germinal center (GC) formations in absence of YY1. AID mediates important GC activities of somatic hypermutations and class-switching of antibodies. I generated yy1flox/flox IgkAID mice that overexpress AID. Ex vivo, genetic deletion of yy1 in these mice resulted in significant reduction of class-switch and a decrease in somatic hypermutation, thus demonstrating that transgenic mice overexpressing AID (IgkAID mice) are still dependent on YY1 to induce class-switch of antibodies to IgG1.