Current PhD vacancies

Animal research Molecular and cell biology Wet lab

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Following fertilization of an oocyte by a sperm, a series of intricate processes is initiated to yield a viable, healthy organism. In humans, initial stages of cell cleavages following fertilization are notably inefficient, with only 30-50% of fertilized oocytes progressing to the blastocyst stage, where the underlying cause is still unclear. In mammals, the oocyte provides all necessary factors for the start of life until the embryo for the first time activates its genome. This activation of embryonic genes occurs species-dependent at the 2-8 cell stage. At early cleavage stages, the embryo retains totipotency, meaning that all its cells possess the capability to contribute to all lineages required for development. Early events guiding the first cellular differentiation in the inner and outer cells of the blastocyst are crucial to setting up the embryo for successful development. The precise timing and critical factors involved in the first differentiation event of mammalian embryos remain incompletely understood. Further research is required to identify the essential factors involved in this process and to elucidate the precise mechanisms underlying the initiation of differentiation during cleavage stages.

Bioinformatics & machine learning Biomedical engineering Computer lab Neuroscience

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The Slak Rupnik lab is seeking a passionate and skilled candidate to contribute to a pioneering project at the intersection of biology, physics, and artificial intelligence. This unique PhD position offers the opportunity to delve into the fascinating world of pancreatic sensory cell collectives and their role in nutrient sensing and metabolic regulation. Pancreatic cells compute their responses to blood level glucose collectively, as an interacting network, much as neurons in the central nervous system do. Our ambitious project aims to revolutionize our understanding of pancreatic sensory cell collectives across various spatio-temporal scales, from cell-cell and islet-islet interactions, integrating insights from blood flow velocities and microvasculature organization. Our approach goes beyond traditional molecular studies, pioneering cutting-edge single cell and real-time functional data-acquisition to uncover the complex orchestration of pancreatic cells in nutrient homeostasis and metabolic response.You will contribute to innovative research at the forefront of physiology and diabetes research, utilize AI-driven models to analyze and predict pancreatic cell behavior, and engage in the development of stochastic biophysical models and reinforcement learning techniques for optimal control in nutrient homeostasis. You will have an opportunity to contribute significantly to a field with immense potential for therapeutic advancement in diabetes. Access to state-of-the-art facilities and resources, including a close and already established collaboration with the biophysics theory & computational neuroscience group at Institute of Science and Technology Austria (http://gtkacik.pages.ist.ac.at).

Animal research Biochemistry & Biophysics Cardiovascular systems Immunology Wet lab

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Extracellular vesicles (EVs) are subcellular particles that are shed by activated cells and cells undergoing programmed cell death. EVs reflect the pathophysiological state of the parental tissues and are important mediators of intercellular and interorgan communication. Increased circulating levels of EVs have been identified in cardiovascular disease, where they are thought to be key modulators of disease progression. We have recently identified a subset of EVs that reflects metabolic state of increased oxidative stress and that are bound by specific receptors of innate immunity. The aim of this project is to characterize the production, trafficking and immune-mediated clearance of these EVs in conditions predisposing to an increased cardiovascular risk, including hyperlipidemia and/or metabolic-dysfunction associated fatty liver disease. Experimental approaches will include multiple omics-based characterization of EVs, cell culture-based functional assays and mouse models of vascular inflammation and myocardial infarction.

Biomedical engineering Cardiovascular systems Human research Wet lab

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Over the last years research has entered a new era by reprogramming cells back into a stem cell-like state and using such cells for three-dimensional tissue engineering to better model human development and disease. 3D organoids have the potential to fill the gap between conventional 2D cultures and animal experimentation, both of which have limitations in terms of bioethics or faithful representation of human physiological processes. The Penninger lab has pioneered the generation of human blood vessel organoids (hBVO) (PMID 30651639) created from induced pluripotent stem cells (iPSCs). These organoids self-assemble into capillary networks containing endothelial and pericyte cells enveloped by a basement membrane. When transplanted into immunodeficient mice, in vivo perfused human vascular organoids specified into arterioles, arteries and venules, allowing us to grow a fully functional human vascular tree in mice. In addition, using BVO based technology, we have now created human bone marrow organoids (hBMOs) which are capable of producing multiple types of human haematopoietic cells (PMID 38374263). We are looking to recruit an enthusiastic PhD student to use these unique platforms and bioengineer hBVOs and hBMOs to study human diseases such as various blood cancers and rare diseases in affecting blood cells to ultimately uncover novel biology and therapeutic targets. You will be Co-supervised by Prof. Josef Penninger and Shane JF Cronin, PhD.

Animal research Bioinformatics & machine learning Molecular and cell biology Wet lab

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The placenta is a vital organ to sustain embryonic development in the utero. The exchange of nutrients, gases, and metabolites as well as the placenta’s endocrine and immunological functions are mediated by a range of highly specialised trophoblast cell types. Multiple placental pathologies are associated with failures in trophoblast differentiation, yet the underlying molecular basis is poorly understood. Our laboratory studies the mechanisms of self-renewal and differentiation in trophoblast stem cells and organoids, with a particular focus on transcriptional regulation. We take an interdisciplinary approach combining molecular biology, biochemistry, genetic manipulations and proteomics. The offered PhD project aims to dissect the molecular function of a novel chromatin regulator during trophoblast cell fate transitions. We will illuminate its workings using trophoblast stem cell and organoid models and a range of -omics techniques (e.g., RNA-seq, ChIP-seq, ATAC-seq, co-IP/MS, etc.). Our findings will not only clarify the transcriptional control of trophoblast specification but may also provide new insights into the molecular aetiology of placental and pregnancy disorders.

Animal research Biochemistry & Biophysics Endocrinology and Metabolism Molecular and cell biology Wet lab

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Cells organize their metabolic reactions into specialized compartments to ensure efficient turnover and prevent undesirable cross-reactions. However, the dynamic intracellular coordination of metabolic pathways that are essential in maintaining cell functions are not well defined. Recent discoveries have challenged traditional beliefs that glycolysis occurs in the cytosol and the citric acid cycle happens in mitochondria, revealing that selected metabolic enzymes venture into the cell's control center, the nucleus. This project aims to explore the world of metabolic processes on the subcellular level, with a focus on the nucleus and how these reactions support vital cellular functions: Cell division, transcriptional regulation, and epigenetic modifications. As a model system, we use the liver's remarkable regenerative potential to understand how metabolic activity in the nucleus can support cell proliferation. The liver is the only organ in the mammalian body that can largely regenerate and in humans, surgical hepatectomy is a common treatment option for various liver diseases. In mice, the liver regeneration process takes about 3 days which makes this model an excellent choice to study the metabolic processes that accompany rapid cell division. Experimental approaches in this project will include mouse models to study in vivo physiology, live cell imaging, molecular biology, and integrative multi-omics (transcriptomics, proteomics, metabolomics). We are looking for a highly motivated PhD student to join our young team at the Center for Pathobiochemistry and Genetics. We seek to create a collaborative and multidisciplinary research environment and use clinically relevant model systems to bridge the gap between fundamental research and its potential application in clinical settings.

Animal research Human research Molecular and cell biology

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The capacity of Retinoic Acid Receptor (RAR) and Vitamin-D-Rezeptor (VDR) ligands to prevent Prostate Cancer (PCa) growth and metastasis and their interaction with other nuclear receptors and their respective ligands: The activity of RAR antagonists is best characterised in PCa. The interactions between RAR and other nuclear receptors in PCa, and their possible synergy for a treatment, are however completely unknown. The objective is thus to investigate whether by interfering with the unexplored thyroid receptor (TRβ) / androgen receptor (AR) /RARg/VDR axis, a novel combination approach for therapies in advanced PCa to eradicate CSCs and their progeny can be introduced. Thyroid hormones can stimulate PCa growth and regulate PCa-specific genes autonomously via TRβ or in conjunction with the AR and/or RXRg. Thus, DC-MUV-2 will study the impact of thyroid hormones on tumour growth using faithful models of extensively characterized PCa models. The detailed role of TRβ will be analysed in human PCa cell lines PCa LnCAP, 22Rv1, DU-145, and PC3 and in 3D mouse PCa organoid models by knockout strategies in vitro and in vivo. Transcriptional activity of the TRβ/AR or TRβ/RAR complex will be tested by analysis of gene promoter activity, nuclear translocation of the respective complexes, and gene expression studies. Tumour growth will be comparatively monitored with and without hypothyroidism in PCa xenograft models in vivo. DC-MUV-2 will then study the effects of anti-thyroid hormone agents with or without anti-AR or RAR and/or VDR ligand compounds in vitro and validate the results in PCa xenograft models. Molecular results will be validated with histopathological analyses in an extensive retrospective cohort of FFPE PCa patient samples to identify patient characteristics that may predict response to thyroid hormone therapy. Results from xenograft models will be analysed with histoplasmonics and forwarded to DC-TG for method development. RNASeq and ChiPSeq analyses will be fed to DC-UoB. Results from new hybrid compounds will be fed back to DC-MUW for structure optimisation.

Animal research Behavioural biology Biochemistry & Biophysics Cancer Molecular and cell biology Wet lab

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We are looking for two highly motivated PhD students to be jointly hosted by the team of Assoc. Prof. Brigitte Hantusch and Prof. Lukas Kenner at the Department of Pathology (Medical University of Vienna) and at the Department of Experimental Animal Pathology (Vetmeduni Vienna). The PhD project will be part of a project for “Role of thyroid hormones and thyroid hormone receptor β in prostate cancer” funded by the “FWF”. The Project: The overarching goal of this project is to elucidate the role of the thyroid hormone signaling pathway for prognosis and therapy response of PCa. We could show that thyroid hormones stimulate PCa growth and that TRβ can regulate PCa-specific genes in conjunction with the androgen receptor (AR). Interfering with this yet unnoted T3/TRβ/AR axis might represent a potential approach for novel therapies in androgen-refractory PCa. We aim to elucidate the TRβ/AR signaling interaction with and without androgen and/or T3 stimulation in vitro and in xenografted PCa mouse models in vivo. The student will measure the transcriptional activity of TRβ and AR complex by promotor gene activity, nuclear translocation and gene expression studies. He/she will further investigate the effects of anti-thyroid agents, validate the results in human xenograft models for PCa and correlate them with histo-pathological and molecular findings in PCa patients to identify those that might benefit from therapeutic targeting of thyroid hormone signaling.

PhD Program: IAI-SHIELD Cancer Human research Immunology Molecular and cell biology Wet lab

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Some CD4⁺ T-cell subsets display cytotoxic activity (CD4 CTLs), thus breaking the functional dichotomy of CD4⁺ helper and CD8⁺ cytotoxic T-cells. CD4 CTLs are generated during viral infections and anti-tumour immunity in humans and mice. Moreover, CD4 CTLs might also cause immunopathology in autoimmune diseases. However, the molecular mechanism regulating their differentiation is poorly understood. Naïve CD4⁺ T-cells transferred into RAG2-KO mice differentiate into CD4⁺CD8aa⁺ CTLs in the small intestine, thus providing an ideal experimental system to study CD4 CTL differentiation. In this PhD project, we will investigate novel mechanisms regulating CD4 CTL differentiation, focusing on epigenetic and transcriptional regulation. Understanding these mechanisms will reveal novel approaches for therapeutic induction of CD4 CTLs.

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

Behavioural biology Biochemistry & Biophysics Molecular and cell biology Wet lab

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To date, more than 150 chemical RNA modifications have been described, most of them found in tRNAs. However, many of their synthesis pathways and their impact on the RNA molecule itself and on the cell remain poorly understood. Remarkably, mutations in about a half of the currently known RNA modification enzymes are associated with human diseases. We will investigate the role of core modifications on tRNA folding and function, and their impact on the cell in physiological and/or pathological conditions. Main Objectives In our lab we investigate the process of tRNA methylation from its multiple faces and aim to address the following fundamental questions: how do modification enzymes work to recognize their substrate? what is the effect of the modification on the tRNA structure/function? what are the consequences of modification, and of its absence, on cellular function?

Immunology Molecular and cell biology Wet lab

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Dental mesenchymal stromal cells (MSCs) are present in different dental tissues and fulfill the minimal MSCs criteria. These cells possess immunomodulatory properties, usually enhanced by cytokines secreted by immune cells. Thus, MSCs and immune cells interact reciprocally and regulate each other’s activity. Vitamin D3 is known to play an important role in bone and mineral homeostasis as well as in the regulation of inflammatory processes. Our recent studies show that different forms of vitamin D3 affect the immunomodulatory properties of dental MSCs. Moreover, the enzymes involved in vitamin D3 metabolism are present in almost all tissues, including dental tissues. In the present project, we will investigate how inhibition of local vitamin D3 conversion influences the regenerative potential and immunomodulatory activity of dental MSCs. We will use the gene-editing technique to alter the expression levels of the key enzymes involved in vitamin D3 activation and how this deletion will influence the physiological properties of dental MSCs. Additionally, we will investigate how different vitamin D3 metabolites affect gene expression in dental MSCs using RNAseq. The expression of key enzymes and metabolites will also be studied in individuals with periodontitis to assess a possible connection between alterations of local vitamin D3 metabolisms and inflammatory diseases.

Animal research PhD Program: IAI-SHIELD Cancer Human research Immunology Molecular and cell biology Wet lab

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The lung microenvironment is composed by structural and immune cells, which together shape the activity and plasticity of tissue resident macrophages. We and others have discovered that rare innate immune cell populations, like ILC2s, eosinophils, basophils or mast cells, regulate the homeostatic phenotype of alveolar macrophages, the functionality of which is essential in the response to respiratory infections. Any alteration in this response can result in impaired defense and/or exaggerated inflatmation upon (viral) infection or injury. Within this project we will follow the hypothesis that ratre innate immune cells contribute to the responsiveness of lung macrophages to viral infections and upon injury. Understanding the intricate interplay of regulatory immune cells and their impact on macrophage functionalities upon viral lung infections will enable us to fine tune immune responeses and prevent severe disease manifestations as currently seen in some COVID-19 patients.

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

PhD Program: IAI-SHIELD Cancer Immunology Molecular and cell biology Wet lab

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In cutaneous lupus erythematosus (CLE) autoreactive T cells play a major role in tissue inflammation and organ damage. Georg Stary has shown that tissue-resident T cells can survive in the tissue independently of the circulation for more than a decade, contribute to inflammation while being therapeutically hard to reach and exit the skin to participate in inflammation in distant organs. The distribution between circulating and tissue-resident T cells in CLE and their specificity remain elusive. Georg Stary will follow the hypothesis that TCR clones of pathogenic T cells recognizing auto-antigens are found within the tissue-resident T cell pool in CLE patients and contribute to systemic disease. Identification of pathogenic tissue-resident T cells, their T cell antigens and specific immunodominant epitopes is crucial for understanding disease pathophysiology and can help designing targeted therapies.

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

Animal research PhD Program: IAI-SHIELD Immunology Molecular and cell biology Wet lab

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Candida albicans is among the most prevalent opportunistic human fungal pathogens and is an important cause of mortality also because of increased drug resistance. It leads to diseases such as disseminated and chronic cutaneous candidiasis, particularly in immunocompromised patients. Lots in known on Candida immunity for systemic and mucosal surface infections, while knowledge about the skin immune defence is limited. The BS group has shown that the absence of the cytokine signal transducing kinase TYK2 improves topical clearance of C. albicans and suppresses dissemination to distal organs. Aim of this project is to address how TYK2 signalling in specific cell types, such as skin-resident T cells, orchestrates the immune defence against cutaneous C. albicans infection. This study will not only contribute to the mechanistic understanding of signalling networks controlling C. albicans skin infections and invasive disease, but may unravel novel and urgently needed immune modulatory treatment options.

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

Animal research PhD Program: IAI-SHIELD Cancer Human research Immunology Molecular and cell biology Wet lab

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The hair follicle is an important mammalian structure and its stem cells are protected by an “immune privilege” mechanism maintained primarily by the absence/low expression of major histocompatibility (MHC)-I, T regulatory cell recruitment and secretion of anti-inflammatory factors. This immune privilege protects from tissue damage and hair loss during inflammation. The Bauer lab could recently show that the epidermal growth factor receptor (EGFR) secures hair follicle integrity during novel hair eruption protecting the body from microbial invasion, tissue destruction and skin inflammation, all manifestations also seen in cancer patients receiving EGFR-inhibitors during targeted anti-cancer therapy and patients with EGFR mutations. Preliminary data identified the breakdown of the immune privilege on EGFR deficient hair follicle stem cells prior to their destruction. In this project we will investigate by which molecular mechanism the hair follicle immune privilege is maintained and protected by using genetically engineered mouse models (GEMMs) lacking EGFR in different epidermal cell compartments, patient biopsies, RNA sequencing, single cell transcriptomic approaches and fluorescence activated cell sorting. This aims to uncover molecular networks and interactions at the basis of immune evasion and to identify therapeutic targets preventing anti-cancer therapy adverse events and scarring hair loss (cicatritial alopecia). Similar immune evasion mechanism might also be exploited by cancer cells and therefore represent novel targets for cancer therapy, which will be studied in parallel using state-of-the-art in vitro and in vivo cancer models.

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

PhD Program: IAI-SHIELD Cancer Immunology Molecular and cell biology Wet lab

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Rheumatoid arthritis (RA) is a chronic inflammatory disease leading to irreversible joint destruction involving various cell types. Although T cell targeted therapies have been shown to be effective, the exact role of CD4+ T cells to inflammation and tissue destruction remains unclear. The laboratory of Michael Bonelli has successfully established a T cell dependent arthritis model. Histological analysis reveal synovial tissue inflammation and joint destruction similarly to RA patients. The research team will therefore investigate if and to which extent CD4+ T cells drive the development of inflammatory joint diseases. Using next generation sequencing technologies from human and mouse samples in combination with functional assays will allow to identify the factors that drive pathogenicity of T cells. Understanding the mechanisms that drive the development of pathogenic T cells and their role in inflammatory arthritis will be crucial to identify new treatment targets and develop T cell targeted therapies.

About this project: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

Animal research PhD Program: IAI-SHIELD Cancer Human research Immunology Molecular and cell biology Wet lab

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The Sibilia Lab at the Center for Cancer Research is using genetically engineered mouse models (GEMMs), patient material, primary cells and organoids to dissect the molecular mechanisms underlying the immune system’s ability to combat cancer.  Our goal is to characterize how oncogenic mutations and epigenetic modifications modulate the tumor microenvironment (TME) to identify novel points of intervention in the TME to reactivate the immune response against tumors. The TME is comprised of various stromal and innate and adaptive immune cells that infiltrate tumors and manipulate immune responses and we have a particular interest in innate cells like dendritic cells (DCs) and various subtypes of myeloid cells (macrophages). A mechanistic understanding of how to modulate these cells to enhance anti-tumor immunity is of fundamental importance to improve immune-based anti-cancer treatment in patients. Our lab employs state-of-the-art technologies and multi-omics approaches: e.g. scRNA-Seq, CHIP/ATAC-Seq, multi-colour flow cytometry, cell sorting, genome engineering (Lentiviral, CRISPR/Cas9), multiplex immunofluorescence.

We have 2 PhD positions addressing the following questions:

• How can we modulate innate immunity to convert cold (immunosuppressive) tumors into hot (immunogenic) tumors?
• How are Ras mutations in tumors conferring therapy resistance via the TME?

About the PhD program: These projects will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

PhD Program: IAI-SHIELD Cancer Computer lab Endocrinology and Metabolism Wet lab

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Gut microbiota modulate the immune system and affect human health, ranging from the response to cancer therapies as well as the onset of autoimmune diseases. Antibody responses against (gut) microbiota have been shown to play a key role in mediating this microbiota-immune axis, with cross-reactive antibodies/molecular mimicry between microbial and human proteins being involved in autoimmune disease. However, the actual antigens recognized by antibodies are vastly unknown. By using a newly developed technology, TV will unravel the functional capacity of this enormous immune repertoire targeting microbiota and investigate their role in modulating cancer immunotherapy response as well as immune mediated diseases (IMDs).

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link

Animal research PhD Program: IAI-SHIELD Cancer Immunology Wet lab

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During chronic infection and tumorigenesis CD8⁺ T cells display progressive loss of effector function, widely known as T cell exhaustion. As a member of the SHIELD doctoral program, my group will elucidate the molecular mechanisms underlying T cell exhaustion, particularly focusing on the transcriptional and epigenetic regulations. We will utilize various immunological methods, cutting edge approaches in molecular biology and mouse genetic tools. Our study might thereby provide insight into novel therapeutic approaches against chronic infection and tumor, given that the epigenetic inflexibility of exhausted T cells is a major barrier for effective immunotherapy. Being embedded in a multidisciplinary educational program in immunology, the successful candidate will gain a deep understanding of T cell-mediated immune responses during the PhD study.

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. The immune system protects our body from external (pathogens) and internal (cancer) threats. The elimination of these threats or a misguided attack on the body's own structures inevitably leads to tissue damage. Therefore, ensuring tissue integrity is of utmost importance in preventing autoimmune diseases, infections, and cancer. To comprehensively address these medically relevant questions requires the close interplay between basic research, data science and clinical science. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link. 

PhD Program: IAI-SHIELD Bioinformatics & machine learning Computer lab Immunology Molecular and cell biology Wet lab

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Transcription of inflammatory response genes is strictly signal-dependent and must be tightly controlled to prevent spurious immune activation and auto-immunity. How this control is achieved given the inherent leakiness and noisiness of transcription is currently poorly understood. The aim of this project is to combine state-of-the-art genomics and computational methods, with machine learning approaches, to identify the molecular mechanisms that limit transcriptional noise at the level of single genes with key functions in controlling and eliciting innate immune responses. Since the mechanisms limiting transcriptional heterogeneity in innate immune cells are currently poorly characterized, the results of this project might have profound implications for both our fundamental knowledge as well as how these risk-factors to auto-immune diseases.

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.

Animal research PhD Program: IAI-SHIELD Bioinformatics & machine learning Cancer Computer lab Human research Immunology Molecular and cell biology Wet lab

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The mechanisms underlying metastasis formation by some but not other tumors are poorly understood. They are influenced by the heterogeneity between individual tumor cells and their complex interaction with the tumor microenvironment and subsequent remodeling of metastatic niches. Besides their immune-suppressive phenotypes, myeloid cells seem particularly important in establishing pre- and metastatic niches, thereby enabling successful colonization and outgrowth of metastasis. Less studied, however, is the role of myeloid cells in establishing anti-metastatic niches that may prevent metastasis. A better understanding of these protective cell interactions is crucial for developing novel therapies that may prevent metastasis in high-risk patients or directly help patients with metastatic disease.

In the Winkler Lab, you will work at the interface of basic cancer research and computational biology and use cutting-edge spatial omics applications to dissect tumor-immune cell interaction networks in metastasis. 

About the PhD program: This project will be studied within the PhD-Program IAI-SHIELD which is about securing host immunity: Elimination versus Destruction. SHIELD is a Doc.Funds program funded by the FWF including 11 principal investigators combining wet lab and data science and offering the unique opportunity to train students to address fundamental biomedical questions pertaining to the protective shield our immune system forms. SHIELD will educate researchers for future precision medicine approaches and the substantial insights obtained from our research program are a prerequisite for improved therapies in the future. To learn more about the program, please follow this link.