Lecturer

Thomas Decker

Teaching Statement

The main aim of my teaching activities is to provide students with a fundamental understanding of the immune system. One of my lectures gives a broad overview of the immune system and how its different components interact to provide protective immunity. A second lecture and a seminar are dedicated to signals and transcriptional control required to move cells of the immune system from a quiescent to an activated state.

Scientific Statement

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.

Biography

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)

Download CV

Spotlights

Transcription factor STAT1 is a macrophage-activating signal integration platform

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.

Gene Promoters integrate NFκB and JAK-STAT signaling

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

Interferons increase the vulnerability to infection by intracellular bacteria

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.

Sex-dependent impact of RNA-helicase DDX3X on immunity against bacteria

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.

    16
    Search on the site...

    office@maxperutzlabs.ac.at

    +43 1 4277 240 01


    Vienna BioCenter
    Dr.-Bohr-Gasse 9, 1030 Vienna