Laurel L. Lenz, Ph.D. Assistant Professor Integrated Department of Immunology Ph.D., University of Washington, Seattle, 1998 National Jewish Medical and Research Center Goodman Building, K510 1400 Jackson Street Denver, CO 80206 Phone: 303.398.1767 E-mail: lenzl@njc.org

My lab studies how early events in host-pathogen interactions affect the regulation of innate immunity and thus disease outcome. As a model pathogen, we use Listeria monocytogenes, a Gram-positive bacterium that can invade and grow within the cytosol of nearly all animal cell types. L. monocytogenes is a common contaminant of processed foods and, when ingested by a pregnant woman, can infect placental tissues and the fetus. Such L. monocytogenes infections have been estimated to cause up to 4% of spontaneous abortions in developed countries.

One aspect of our current research investigates the interactions between infected cells and a specific type of innate immune lymphocyte, the natural killer (NK) cell. NK cells are present in the blood (pNK), and are also prevalent in the maternal deciduas during pregnancy (uNK). pNK cells contribute to immune responses during infections and cancer, whereas uNK cells contribute to the development of the maternal and fetal blood systems during formation of the placenta. We are currently investigating how specific microbial and host immune factors influence the activation of each of these NK cell populations in the context of L. monocytogenes infection. Future studies will investigate how such activation affects maternal tolerance of the fetus and pregnancy outcomes.

Selected Publications

Lenz, L. L., Butz, E. A, and Bevan, M. J. (2000) "Requirements for bone marrow-derived antigen-presenting cells in priming cytotoxic T cell responses to intracellular pathogens." J. Exp. Med. 192:1135-1142

Auerbuch, V. A., Lenz, L. L., and Portnoy, D. A. (2001) "Development of a competitive index assay to evaluate the virulence of Listeria monocytogenes actA mutants during primary and secondary infection of mice." Infect. Immun. 69:5953-5957

Lenz, L. L., and Portnoy, D. A. (2002) "Identification of a second L. monocytogenes secA gene that contributes to secretion and is associated with the rough phenotype." Molec. Microbiol. 45:1043-1056.

Lenz, L. L., Mohammadi, S., Geissler, A., and Portnoy, D. A. (2003) "SecA2-dependent secretion of autolytic enzymes promotes Listeria monocytogenes pathogenesis." Proc. Nat. Acad. Sci. 100:12432-12437.

Ploss, A., Lauvau, G., Contos, B., Kerksiek, K. M., Guirnalda, P. D., Leiner, I., Lenz, L. L., Bevan, M. J., and Pamer, E. G. (2003) "Promiscuity of MHC class Ib restricted T cell responses." J. Immunol. 171:5948-5955.

Diehl, G.E, Yue, H.H., Hsieh, K., Ho, M., Kuang, A.A., Morici, L.A., Lenz, L.L., Cado, D., Riley, L.W., Winoto, A. (2004) "TRAIL-R as a negative regulator of innate immune responses." Immunity. 21:877-889.

Arrunategui-Correa, V., Lenz, L., and Kim, H.S. (2004) "CD1d-independent regulation of NKT cell migration and cytokine production upon Listeria monocytogenes infection. Cellular Immunology. 232:38-48.

Latest Publications in PubMed