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Laurel Lenz, Associate Professor

Ph.D. (1998) University of Washington, Seattle



Integrated Department of Immunology

National Jewish Health
Goodman Building, K510
1400 Jackson Street
Denver, CO 80206
Phone: 303-398-1767
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.

  • Humann JL, Bjordahl R, Andreasen K, and Lenz LL. (2007) “Expression of the p60 autolysin enhances NK cell activation and is required for Listeria monocytogenes expansion in IFNg-responsive mice.”  J. Immunol. 178:2407-14

  • Lenz LL, and Andrews-Polymenis HL. (2008) “Silencing the Alarm: Insights into the Interaction Between Host and Pathogen.”  EMBO Reports. 9:27-32.

  • Humann J. and Lenz LL. (2009) “Bacterial peptidoglycan degrading enzymes and their impact on host muropeptide detection.” J. Innate Immun. 1:88-97.

  • Rayamajhi M, Humann J, Penheiter K, Andreasen K, and Lenz LL. (2010) “Induction of IFNab enables Listeria monocytogenes to suppress macrophage activation by IFNg.” J. Exp Med. 207:327-37.

  • Humann J, and Lenz LL. (2010) “Activation of naïve NK cells in response to Listeria monocytogenes requires IL-18 and contact with infected dendritic cells.” J. Immunol. 184:5172-8.

  • Rayamajhi M, Humann J, Kearney S, Hill KK, and Lenz LL. (2010) “Antagonistic crosstalk between type I and II interferons and increased host susceptibility to bacterial infections.” Virulence. 1(5):421-425.

  • Boudreau J, Stephenson K, Wang F, Ashkar A, Mossman K, Lenz LL, Rosenthal K, Bramson J, Lichty B, and Wan Y (2011) “IL-15 and type I interferon are required for activation of tumoricidal NK cells by virus-infected dendritic cells.” Cancer Res. 71(7):2497-506.

  • Rayamajhi M, Redente EF, Condon TV, Gonzalez-Juarrero M, Riches DWH, and Lenz LL. (2011) “Non-surgical intratracheal instillation of mice with analysis of lungs and lung draining lymph nodes by flow cytometry.” J. Vis. Exp. e2702

  • Lei J, Hill, KK, Filak, H., Mogan, J., Knowles, H., Zhang, B., Perraud, A.L., Cambier J, and Lenz LL. (2011) “MPYS is required for IRF3 activation and type I IFN production in the response of cultured phagocytes to bacterial second messengers c-di-AMP and c-di-GMP.” J. Immunol. 187:2595.

  • Schmidt RL, Filak HC, Lemon JD, Potter, TA, and Lenz LL. (2011) “A LysM and SH3-domain containing region of the Listeria monocytogenes p60 protein stimulates accessory cells to promote activation of host NK cells.” PLoS Pathogens 7:e1002368.


Latest Publications in PubMed​​​