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Welcome to the Integrated Department of Immunology at the University of Colorado - School of Medicine and National Jewish Health.

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Laurel Lenz PhD

Associate Professor of Immunology, Microbiology, BSP, and Reproductive Sciences

 Laurel Lenz






Education: Ph.D. University of Washington, Fellowship U.C. Berkeley
Dr. Lenz's National Jewish Health webpage

We use bacterial infection models to dissect molecular mechanisms for immune subversion and immune dysregulation. One aspect of our work focuses on understanding pathogenic strategies that microbes have evolved to thwart or manipulate immune responses. Another aspect is to understand host immune regulatory circuits that are manipulated by pathogens. We are interested in how each of these aspects impacts the ability pathogens to establish mucosal and systemic infections. We are also keenly interested in translating information from our studies into improved therapies for infectious, inflammatory, cancerous, and other diseases.

One current focus is on understanding the mechanisms by which specific bacterial proteins impact the activity of host innate immune cells, including macrophages, dendritic cells, and natural killer (NK) cells. We have identified a LysM-domain containing bacterial protein that triggers immune cell activation. We are interested in the mechanisms for such activation and in understanding how this immune activation benefits the pathogen. We are also interested in development of such immune activating factors for treatment of infections and cancers.

A second focus is on understanding the mechanisms and consequences of crosstalk between endogenous host cytokines. Cytokines such as type I interferons (IFN-ab) and interleukin 10 (IL-10) can suppress the activation of macrophages and other myeloid cells, and increase host susceptibility to a variety of bacterial infections. We are interested in how microbes induce production of these suppressive cytokines and how IFN-ab suppress myeloid cell activation. We recently found that IFN-ab reduce myeloid cell expression of receptors for activating cytokines such as IFNg. Additional mechanistic information on this process may be useful in developing host-directed therapies for infection and for improving the safety of IFN-ab based therapies for multiple sclerosis and other diseases.

The lab uses a variety of mouse models. Model pathogens include the bacteria Listeria monocytogenes and Francisella tularensis, both of which access and replicate in the cytosol of host phagocytes.

  • 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.

View of Recent Publications in PubMed