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Defense against microbial pathogens is based on both pre-existing and ontogenetically acquired mechanisms, with the former forming the innate immune response and the latter known as acquired or adaptive immunity. Both innate and acquired immunity make use of a large group of polypeptides called cytokines to adapt the responsiveness of individual cells and organs to the specific needs of host defense. Interferons (IFN) form a subgroup of cytokines. We devote much effort to the question how interferons change gene expression of cells to produce cell-autonomous immunity. This involves activation of transcription factors by the JAK-STAT signal transduction pathway. In addition we study how the loss of the IFN system impacts on the innate immunity of cells and mice.
We use biochemical and proteomic tools to study signaling via the JAK-STAT pathway. Changes of promoter occupancy, chromatin structure and gene expression are examined by NGS-based technologies. In addition, we use mouse genetics to determine how the loss of responsiveness to IFN impacts on host resistance against intracellular bacteria. Current approaches towards this question include changes in host cytokine production, effector cell survival and cell metabolism.
Professor of Immunobiology at the University of Vienna since 2002. Until 2009 chair of the Department of Microbiology and Genetics
Member of the MCB (since 2012) and JBC (since 2015) editorial boards, editor for the Journal Medical Microbiology and Immunology
President of the European Society for Macrophage and Dendritic Cell Research (EMDS, since 2018)
Dr. Bohr-Gasse 9
1030 Vienna
Room: 4.112
+43-1-4277-54605
Macrophage activation by microbe-induced signals and signals by the IFN-γ receptor (JAK-STAT signaling) converge on transcription factor STAT1. The former move STAT1 to the nucleus whereas the latter modulate its transcription factor activity. Kovarik et al. (1998) EMBO J. 17, 3660-3668. Kovarik et al. PNAS (1999) 96, 13956-13961. Varinou et al. Immunity (2003) 19, 793-802.
Microbial infection causes type I IFN synthesis and JAK-STAT signaling. In addition, the NFκB pathway is activated. The two pathways perform complementary functions in transcriptional initiation such as recruiting the mediator complex and the kinases phosphorylating RNA polymerase. This results in a synergistic effect on gene expression. Farlik et al. (2010) Immunity 33:25-34. Wienerroither et al. (2015) Cell Reports 12: 300-312
Type I IFN, produced during infection with the intracellular bacterium Listeria monocytogenes increase the death of infected macrophages. Likewise, mice are more resistant to L. monocytogenes if a type I IFN response is prevented. Stockinger et al. J. Immunol. (2002) 169, 6522-6529. Stockinger et al. PLoS Pathogens (2009) 5(3): e1000355.
The X-chromosome-encoded enzyme provides antibacterial immunity by increasing transcription of antimicrobial genes. Loss of DDX3X is tolerated in the male immune system due to a y-chromosomal homologue, DDX3Y. Female cells have a strongly reduced life span and female mice lacking DDX3X in the immune system die in utero. Soulat et al. EMBO J. (2008) 27:2135-2146. Szappanos et al. PLoS Pathogens (2018) 14(11): e1007397.
Olga Babadei
PhD Student +43-1-4277-54628
Room: 4.522/4.524
Andreas Brandauer
Diploma/Master Student +43-1-4277-24001
Room: 4.522/4.524
Thomas Decker
Group Leader +43-1-4277-54605
Room: 4.112
Birgit Rapp
Lab Manager +43-1-4277-54628
Room: 4.522/4.524
Fotima Touraeva
Technician +43-1-4277-
Room: 4.522/4.524
Role of Tissue Protection in Lethal Respiratory Viral-Bacterial Coinfection.
Jamieson, Amanda M; Pasman, Lesley; Yu, Shuang; Gamradt, Pia; Homer, Robert J; Decker, Thomas; Medzhitov, Ruslan
Noncanonical effects of IRF9 in intestinal inflammation: more than type I and type III interferons.
Rauch, Isabella; Rosebrock, Felix; Hainzl, Eva; Heider, Susanne; Majoros, Andrea; Wienerroither, Sebastian; Strobl, Birgit; Stockinger, Silvia; Kenner, Lukas; Müller, Mathias; Decker, Thomas
Cooperative Transcriptional Activation of Antimicrobial Genes by STAT and NF-κB Pathways by Concerted Recruitment of the Mediator Complex.
Wienerroither, Sebastian; Shukla, Priyank; Farlik, Matthias; Majoros, Andrea; Stych, Bernadette; Vogl, Claus; Cheon, HyeonJoo; Stark, George R; Strobl, Birgit; Müller, Mathias; Decker, Thomas
The Group Decker participates in the Special Research Area (SFB) "Jak-Stat Signaling: from Basics to Disease" funded by the Austrian Science Fund FWF. SFB's are peer-reviewed, highly interactive research networks, established to foster long-term, interdisciplinary co-operation of local research groups working on the frontiers of their thematic areas.
The Group Decker is a member of the special Doctoral Program "Signaling Mechanisms in Cellular Homeostasis" reviewed and funded by the Austrian Research Fund FWF.
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