Honors & Awards

  • Marie Sklodowska-Curie Fellowship, European Comission Program EU?s Horizon 2020 (2018)
  • Best PhD Award, Hannover Medical School (2017)
  • Travel grant for International Congress of Immunology, Melbourne, Australia, EU Federation of Immunological Societies (EFIS) (2016)
  • Travel grant for the Annual meeting of the Society, German Virological Society (2016)
  • Travel grant for Annual Meeting of Middle-European Societies for Immunology and Allergology, University of Rijeka Foundation (2013)

Professional Education

  • Diploma, University of Ljubljana (2010)
  • Doctor of Philosophy, Hanover School of Medicine (2016)

Stanford Advisors


All Publications

  • Activation of Innate and Adaptive Immunity by a Recombinant Human Cytomegalovirus Strain Expressing an NKG2D Ligand PLOS PATHOGENS Tomic, A., Varanasi, P. R., Golemac, M., Malic, S., Riese, P., Borst, E. M., Mischak-Weissinger, E., Guzman, C. A., Krmpotic, A., Jonjic, S., Messerle, M. 2016; 12 (12)


    Development of an effective vaccine against human cytomegalovirus (HCMV) is a need of utmost medical importance. Generally, it is believed that a live attenuated vaccine would best provide protective immunity against this tenacious pathogen. Here, we propose a strategy for an HCMV vaccine that aims at the simultaneous activation of innate and adaptive immune responses. An HCMV strain expressing the host ligand ULBP2 for the NKG2D receptor was found to be susceptible to control by natural killer (NK) cells, and preserved the ability to stimulate HCMV-specific T cells. Infection with the ULBP2-expressing HCMV strain caused diminished cell surface levels of MHC class I molecules. While expression of the NKG2D ligand increased the cytolytic activity of NK cells, NKG2D engagement in CD8+ T cells provided co-stimulation and compensated for lower MHC class I expression. Altogether, our data indicate that triggering of both arms of the immune system is a promising approach applicable to the generation of a live attenuated HCMV vaccine.

    View details for DOI 10.1371/journal.ppat.1006015

    View details for Web of Science ID 000392202100014

    View details for PubMedID 27907183

    View details for PubMedCentralID PMC5131914

  • Inflammatory monocytes and NK cells play a crucial role in DNAM-1-dependent control of cytomegalovirus infection JOURNAL OF EXPERIMENTAL MEDICINE Rovis, T. L., Brlic, P. K., Kaynan, N., Lisnic, V. J., Brizic, I., Jordan, S., Tomic, A., Kvestak, D., Babic, M., Tsukerman, P., Colonna, M., Koszinowski, U., Messerle, M., Mandelboim, O., Krmpotic, A., Jonjic, S. 2016; 213 (9): 1835-1850


    The poliovirus receptor (PVR) is a ubiquitously expressed glycoprotein involved in cellular adhesion and immune response. It engages the activating receptor DNAX accessory molecule (DNAM)-1, the inhibitory receptor TIGIT, and the CD96 receptor with both activating and inhibitory functions. Human cytomegalovirus (HCMV) down-regulates PVR expression, but the significance of this viral function in vivo remains unknown. Here, we demonstrate that mouse CMV (MCMV) also down-regulates the surface PVR. The m20.1 protein of MCMV retains PVR in the endoplasmic reticulum and promotes its degradation. A MCMV mutant lacking the PVR inhibitor was attenuated in normal mice but not in mice lacking DNAM-1. This attenuation was partially reversed by NK cell depletion, whereas the simultaneous depletion of mononuclear phagocytes abolished the virus control. This effect was associated with the increased expression of DNAM-1, whereas TIGIT and CD96 were absent on these cells. An increased level of proinflammatory cytokines in sera of mice infected with the virus lacking the m20.1 and an increased production of iNOS by inflammatory monocytes was observed. Blocking of CCL2 or the inhibition of iNOS significantly increased titer of the virus lacking m20.1. In this study, we have demonstrated that inflammatory monocytes, together with NK cells, are essential in the early control of CMV through the DNAM-1-PVR pathway.

    View details for DOI 10.1084/jem.20151899

    View details for Web of Science ID 000382520900014

    View details for PubMedID 27503073

    View details for PubMedCentralID PMC4995080

  • Cytomegalovirus m154 Hinders CD48 Cell-Surface Expression and Promotes Viral Escape from Host Natural Killer Cell Control PLOS PATHOGENS Zarama, A., Perez-Carmona, N., Farre, D., Tomic, A., Borst, E. M., Messerle, M., Jonjic, S., Engel, P., Angulo, A. 2014; 10 (3)


    Receptors of the signalling lymphocyte-activation molecules (SLAM) family are involved in the functional regulation of a variety of immune cells upon engagement through homotypic or heterotypic interactions amongst them. Here we show that murine cytomegalovirus (MCMV) dampens the surface expression of several SLAM receptors during the course of the infection of macrophages. By screening a panel of MCMV deletion mutants, we identified m154 as an immunoevasin that effectively reduces the cell-surface expression of the SLAM family member CD48, a high-affinity ligand for natural killer (NK) and cytotoxic T cell receptor CD244. m154 is a mucin-like protein, expressed with early kinetics, which can be found at the cell surface of the infected cell. During infection, m154 leads to proteolytic degradation of CD48. This viral protein interferes with the NK cell cytotoxicity triggered by MCMV-infected macrophages. In addition, we demonstrate that an MCMV mutant virus lacking m154 expression results in an attenuated phenotype in vivo, which can be substantially restored after NK cell depletion in mice. This is the first description of a viral gene capable of downregulating CD48. Our novel findings define m154 as an important player in MCMV innate immune regulation.

    View details for DOI 10.1371/journal.ppat.1004000

    View details for Web of Science ID 000337470300043

    View details for PubMedID 24626474

    View details for PubMedCentralID PMC3953435

  • Superior induction and maintenance of protective CD8 T cells in mice infected with mouse cytomegalovirus vector expressing RAE-1 gamma PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Trsan, T., Busche, A., Abram, M., Wensveen, F. M., Lemmermann, N. A., Arapovic, M., Babic, M., Tomic, A., Golemac, M., Brinkmann, M. M., Jaeger, W., Oxenius, A., Polic, B., Krmpotic, A., Messerle, M., Jonjic, S. 2013; 110 (41): 16550-16555

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