Assistant Professor of Microbiology
| Address: | 1825 University Blvd Shelby Building, room 411 UAB Birmingham, AL 35294 |
| Telephone: | 205-975-7150 |
| Email: | rgking@uab.edu |
| Publications |
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Education
B.S. (Chemistry/Biochemistry), University of Arkansas, 2000
Ph.D. (Microbiology) University of Alabama at Birmingham, 2007
Postdoctoral Training, University of Alabama at Birmingham, 2007-2011
Research Interests
My research is focused on understanding the molecular mechanisms involved the generation and maintenance of humoral immunity. We use a variety of genetically engineered murine models and model antigens to investigate the germinal center process and the generation of long lived memory B lymphocytes and plasma cells. My recent work has focused on the role of the adaptor protein HSH2 in the generation of class switched plasma cells. HSH2 is upregulated by B lymphocytes in response to factors that promote their activation, survival and differentiation. It is first expressed at the protein level by late transitional B cells and its expression is maintained in all follicular B lymphocytes. B cells within the germinal center, however, down regulate HSH2. Using HSH2 hypomorphic and transgenic mice we have demonstrated HSH2 expression rheostatically controls the generation of isotype switched antibody production. We are currently investigating the molecular mechanisms of this effect. Additionally I am involved in studies to determine the function of Intraflagellar transport proteins in B lymphocytes. The intraflagellar transport system (IFT) is a microtubule motor based transport system responsible for both the formation and maintenance of cilia. Lymphocytes are among the few cell types within mammalian systems that do not possess primary cilia. However, recent studies demonstrate that B cells express IFT proteins, which suggest cilia independent functions of the IFT system in immune cells. By crossing mice harboring conditional deletions of IFT genes with CD19cre animals we have developed a murine model with a B cell specific deficiency of IFT proteins. Preliminary studies demonstrate that these mice display a reduction in antigen specific isotype switched antibody following immunization with T-dependent antigen. Furthermore, B cells isolated from these animals produce significantly less antibody, especially of switched isotypes, in response to a range of stimuli in vitro. These data suggest that components of the IFT system play an important role in regulating humoral immunity and that the components of the IFT may have cellular functions in addition to their well described roles in the formation and maintenance of cilia.