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B.S., The Ohio State University, Columbus, OH 2012
Honors and Awards:
The focus of my thesis research is the early drivers of T follicular helper (Tfh) cell differentiation. Tfh cells mediate protective antibody responses by promoting the generation of long-lived plasma cells and memory B cells, thereby dictating vaccine efficacy. Dendritic cells initiate Tfh differentiation while B cells are required for their maintenance. We have identified a significant role for T cell receptor signal (TCR) strength in the generation of Tfh cells at the peak of Listeria infection. We hypothesize that differences in TCR signal strength affect the initial dendritic cell-mediated Tfh differentiation. We are testing this hypothesis with B3K506 and B3K508 TCR transgenic CD4+ T cells, which express TCRs with different affinities for 3K peptide:major histocompatibility complex II. These T cells allow us to examine whether different TCR affinities for the same p:MHCII alter the initial bifurcation into T helper 1 or Tfh cells following Listeria expressing 3K peptide infection. The effect of TCR signal strength on the bifurcation can be driven by variety of pathways downstream of TCR signaling, like cytokine receptor expression. Currently, we are examining the TCR regulated expression of the cytokine receptor IL-2Ra and how this differential expression is affecting the bifurcation. We are also studying the affect of TCR affinity on T cell interactions with dendritic cells in the initial hours of an immune response and how these interactions influence the bifurcation. Collectively, my thesis research will provide insights into early Tfh differentiation thereby providing basic rules for the type of immune response that needs to be generated by a vaccine for optimal T cell help to B cells.