Source: Interfolio F180
John Teijaro
Research Focus
My focus is on studying persistent viral infection using the LCMV system and acute viral pathogenesis utilizing the influenza virus in a mouse model. I have been trained in the growing and titrating LCMV as well as infecting mice with various LCMV clones. I have experience quantifying and analyzing functionality of virus specific T cells. I am currently investigating the role type 1 interferon plays in the initiation and maintenance of persistent virus infection and how type 1 interferon signaling promotes cytokine amplification and immune pathology during influenza virus infection. I have experience working at the interface of virology and immunology. During my graduate studies I set up an influenza virus infection system to investigate memory CD4 T cells responses to influenza virus infection in mice with Donna Farber. With Donna I identified that memory CD4 T cells contribute to both protection and immune pathology following influenza virus challenge. We demonstrated that memory CD4 T cells could provide protection independently of CD8 T cells or B cells by a mechanism requiring IFN-?. Moreover, we were the first lab to demonstrate the existence of tissue resident memory CD4 T cells in the lung and that these resident memory T cells provided optimal protection to influenza virus re-challenge. I continued my training in viral immunology by gaining expertise in both the LCMV and Influenza virus systems with Michael Oldstone. During my time in Michael’s laboratory, I shifted my focus in two directions, 1) towards innate immune responses and understanding how innate cytokine amplification during influenza virus infection contributes to disease pathogenesis and 2) studying how the immune system controls persistent LCMV (clone-13) infection. My work on cytokine amplification during influenza virus infection resulted in the surprising finding that endothelial (not epithelial) cells were central regulators of cytokine amplification during influenza virus. Moreover, blunting this cytokine amplification during human pathogenic influenza virus infection resulted in improved survival, demonstrating for the first time that innate immune pathology is causal in influenza virus pathogenesis. The future directions focus on understanding the pulmonary cellular players that initiate and amplify cytokines/chemokines following influenza virus challenge. Further, we recently demonstrated that blockade of type 1 interferon signaling during persistent LCMV infection resulted in hastened clearance of persistent LCMV from mouse hosts. We demonstrate that blockade of type 1 interferon (IFN-I) signaling using a type 1 interferon receptor neutralizing antibody reduced immune system activation, decreased expression of negative immune regulatory molecules, and restored lymphoid architecture in mice persistently infected with lymphocytic choriomeningitis virus (LCMV). IFN-I blockade both prior to and following establishment of persistent virus infection resulted in a CD4-T cell dependent enhanced virus clearance. We demonstrate a direct causal link between IFN-I signaling, immune activation, negative immune regulator expression, lymphoid tissue disorganization and virus persistence.
Education
B.S. (Molecular & Cell Biology), Millersville University of Pennsylvania, 2004Ph.D. (Microbiology & Immunology), University of Maryland, 2009
Awards & Professional Activities
2006 Minority Travel Award, American Association of Immunologists2007 Minority Travel Award, Keystone Symposia
2007 Minority Travel Award, American Association of Immunologists
2008 Minority Travel Award, FASEB/AAI
2008 Trainee Abstract Award, American Association of Immunologists
2008 Ollie Aylar Award, University of Maryland
2010 Trainee Abstract Award, American Association of Immunologists
2011 1st Prize for Best Fellows Talk, The Scripps Research Institute, IMS Research Forum
2014 Faculty Scholar, Donald E. and Delia B. Baxter Foundation
Selected Publications
Zak, J.; Teijaro, J. R.; Pratumchai, I.; Oldstone, M. B.; Min, B.; Huang, Z. B cell-derived IL-27 promotes control of persistent LCMV infection.. Proceedings of the National Academy of Sciences of the United States of America 2022, 119.
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Woehl, J. L.; Vartabedian, V. F.; Thompson, A. J.; Teijaro, J. R.; Paulson, J. C.; Kikuchi, C.; Edgar, L. J. Sialic Acid Ligands of CD28 Suppress Costimulation of T Cells.. ACS central science 2021, 7, 1508-1515.
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Teijaro, J. R.; Teijaro, J. R.; Monjazeb, A. M.; Mcgee, H. M.; Marciscano, A. E.; Kaech, S. M.; Campbell, A. M. Parallels Between the Antiviral State and the Irradiated State.. Journal of the National Cancer Institute 2021, 113, 969-979.
Teijaro, J. R.; Teijaro, J. R.; Shaabani, N.; Paessler, S.; Maruyama, J.; Manning, J. T.; Ji, H.; Janda, K. D.; Eubanks, L. M.; Blake, S.; Beutler, N. Salicylanilides Reduce SARS-CoV-2 Replication and Suppress Induction of Inflammatory Cytokines in a Rodent Model.. ACS infectious diseases 2021, 7, 2229-2237.
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Zhang, Y.; Xian, H.; Trudler, D.; Tourtellotte, W. G.; Torre, J. C.; Teijaro, J.; Soroosh, P.; Sanchez-lopez, E.; Nilsson, A. R.; Luevanos, M.; Liu, Y.; Lipton, S. A.; Lewis, G.; Karin, M.; Kang, S.; Gatchalian, R.; Crother, T. R.; Chen, W.; Arditi, M.; Aleman-muench, G. R. Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation.. Immunity 2021, 54, 1463-1477.e11.
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Burton, D. R.; Teijaro, J. R.; Schultz, P. G.; Yang, L.; Woods, A. K.; Wolff, K. C.; Vargas, N.; Teijaro, J. R.; Shaabani, N.; Schultz, P. G.; Sahoo, D.; Rogers, T. F.; Roberts, A. J.; Riva, L.; Ricketts, J.; Parren, M.; Pan, K.; Nguyen, T. H.; Mcnamara, C. W.; Kuo, P.; Kirkpatrick, M. G.; Joseph, S. B.; Hull, M. V.; Huang, E.; Gupta, A. K.; Ghosh, P.; Garcia, E.; Fuller, M.; Das, S.; Chi, V.; Chen, E. I.; Chatterjee, A. K.; Burton, D. R.; Beutler, N.; Bakowski, M. A.; Anil, G. Drug repurposing screens identify chemical entities for the development of COVID-19 interventions.. Nature communications 2021, 12, 3309.