Lena Artner-Gent
Group: Maria Sibilia
E-Mail: lena.artner@meduniwien.ac.at
ORCID: 0000-0003-4299-7542
Your epithelial barriers are the first line of defense against pathogens. However, the mechanisms of keeping the balance between efficient immune responses against invading species and the prevention of auto inflammatory diseases is still incompletely understood. I am interested in elucidating how cancer treatment effects the barrier functions in regard of handling bacterial invasion and tolerance to its microbiome.
Hossein Arzani
Group: Karl Kuchler & Arndt von Haeseler
E-Mail: hossein.arzani@meduniwien.ac.at
ORCID: 0000-0002-8077-7586
T helper cells (Th) are crucial part of the adaptive system and their subsets are wide in function. Moreover, the Th9 subset which are predominately known for their IL-9 production are characterized poorly. This subset resides in the mucosal surfaces and are vastly found in the skin. The main activators of these cells are pathogenic fungi which will be my main focus during my research. I would like to use both computational and biological analysis to take a closer look at the characterization of the Th9 cells and their interaction with pathological fungi.
Alfredo Cristiano De Sa Fernandes
Group: Maria Sibilia
E-Mail: alfredo.desafernandes@meduniwien.ac.at
ORCID: 0000-0002-2863-8458
Epigenetic modifications have been increasingly associated with modulation of immune responses, however how this is mediated and their consequences in vivo remain largely unknown. In this project, I aim to understand whether epigenetic immune-regulation can affect the function of immune cells in tumors.
Gülnihal Kavaklioglu
Group: Christian Seiser
E-Mail: guelnihal.kavaklioglu@meduniwien.ac.at
ORCID: 0000-0001-8936-5599
DNA methylation is one of the main epigenetic mechanisms playing a role in establishment of cell identity. DNA methyltranferase 1 (DNMT1) is the maintenance methyltransferase functioning during cell division to preserve methylation patterns in the daughter cells. My research interest focuses on how DNMT1 regulates macrophage activation and polarization in the innate immune system. Using conditional knock-out mouse models, I aim to delineate the mechanisms by which DNMT1 modulates macrophage phenotype.
Alina Leuchtenberger
Group: Arndt von Haeseler
E-Mail: alina.leuchtenberger@univie.ac.at
ORCID: 0000-0003-2566-4260
Artificial Neural Networks can be used to solve various data processing tasks in the field of biology. Although they are mathematical functions these functions are too complex to be intuitively understood by humans. My project is to find methods to analyse and interpret Artificial Neural Networks in a more intuitive way.
Trinh Phan Canh
Group: Karl Kuchler
E-mail: phancanht99@univie.ac.at
ORCID: 0000-0002-6399-0959
Fungal infections are under-recognized hidden killers in infectious diseases, since they claim about 1.5 million human lives per year, with Candida species representing the most prevalent fungal pathogens. Candida auris is a newly emerging fungal pathogen, showing untreatable clinical resistance to all known antifungal drugs. This project applies an integrated poly-omics strategy to discover pathogenesis mechanisms of C. auris. We hypothesize that morphogenesis and metabolic genes control drug resistance and virulence traits of C. auris that promote host colonization and immune evasion. Based on comparative data between different clinical multidrug-resistant C. auris strains, we identify inter-twined mechanisms of morphogenesis, adhesion as well as invasion using in vivo mouse and ex vivo human skin infection models.
Sara Miranda
Group: Birgit Strobl
E-Mail: SaraCatarina.daSilvaMiranda@vetmeduni.ac.at
ORCID: 0000-0002-4717-7669
During my PhD I will investigate enzymatic and scaffolding functions of TYK2, a member of the Janus kinase (JAK) family. I will use Tyk2-deficient mice and TYK2 kinase-inactive mice to unravel TYK2 kinase-dependent and -independent functions during skin infection with Candida albicans. Moreover, I will use newly available TYK2 inhibitors to complement the studies with gene-targeted mice.
Ramona Rica
Group: Wilfried Ellmeier
E-Mail: ramona.rica@meduniwien.ac.at
ORCID: 0000-0001-5501-8513
My project focuses on investigating the role of histone deacetylases (HDACs) in tissue resident lymphocyte-like cells, known as innate lymphoid cells (ILCs). ILCs play an important role in protective immunity and can maintain tissue homeostasis and barrier integrity. Transcriptional networks regulating ILC differentiation and effector function are conserved between ILCs and T cells. Since HDACs are crucial regulators of T cell function, we hypothesize that HDACs regulate ILC subtype differentiation and effector function and that loss of HDACs in ILCs might influence tissue homeostasis and immunity. This hypothesis will be tested in my PhD project.
Jana Trifinopoulos
Group: Veronika Sexl
E-Mail: Jana.Trifinopoulos@vetmeduni.ac.at
ORCID: 0000-0003-3163-5001
Cyclin-dependent kinase (CDK) 8 is an important transcriptional regulator. Recently, it was identified as an oncogene in different types of cancer and suppressive to natural killer (NK) cell antitumor response. Our aim is to elucidate the molecular mechanism underlying this restraining effect of CDK8 in NK cells.
Irina Tsymala
Group: Karl Kuchler
E-Mail: irina.tsymala@meduniwien.ac.at
ORCID: 0000-0002-8515-5209
Innate lymphoid cells are newly identified key players in tissue homeostasis. They preferentially reside at specific mucosal tissues, contributing to the first line of defense against invasive pathogens. Fungi colonize mucosal barrier tissues in the healthy human body in a commensal-like manner, but can turn into dangerous pathogens in immune compromised individuals. My goal is to further elucidate molecular mechanisms that regulate the ILC response to pathogenic fungi.
Rajagopal Varada
Group: Michael Jantsch
E-Mail: rajagopal.varada@meduniwien.ac.at
ORCID: 0000-0001-6740-6564
Adenosine to inosine deamination by ADARs is the most abundant type of RNA editing in metazoans. A-to-I RNA editing has been shown to play an essential role in mammalian embryonic development and tissue homeostasis. ADAR-mediated editing of endogenous dsRNAs is critical to distinguish self- from non self-RNAs. Further, A to I RNA editing recodes proteins essential for tissue homeostasis. The aims of the project are, 1) to identifying the endogenous RNAs that activate antiviral responses in the absence of A to I editing , and 2) to determine the impact of protein recoding on tissue homeostasis and microbiome dysbiosis in intestinal inflammation.