The effect of CD43 on T cell motility

Friday, October 28, 2011
Hall 1-2 (San Jose Convention Center)
Claudia Espinoza , Biology, University of New Mexico, Albuquerque
Ivy Brown, BS , Biology, University of New Mexico, Albuquerque, NM
Judy Cannon, PhD , Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, NM
The immune system provides defense against pathogenic microbes. Multiple specialized cells, including B and T cells, macrophages, dendritic cells and others, work together to eradicate infections . T cells encounter antigen presenting cells in lymph nodes leading to activation. Once activated, T cells are able to activate B cells, improve macrophage function, and kill pathogen infected cells. An important characteristic of T cells is their ability to migrate first to lymph nodes and then to sites of infection in order to activate and then eliminate pathogens. Our laboratory is interested in the molecules that control T cell migration. We have previously shown that a molecule on the T cell surface, CD43, affects T cell trafficking by phosphorylation of S76 within its cytoplasmic tail. We are now interested in defining how CD43 specifically influences T cell motility. Using live cell microscopy, we are generating time lapse videos of migrating T cells isolated from wild type and CD43-deficient mice and comparing the motility of normal versus CD43-deficient T cells. Our experiments will determine if CD43 impacts T cell speed and directionality.