Currently Open Positions

Natural killer (NK) cells are an important component of the innate immune system. Upon activation, NK cells have the potential to lyse damaged or infected cells as well as to secrete an array of inflammatory cytokines and chemokines which may act to both control infection and/or recruit cells to the site of activation.  Unlike other major lymphocyte subsets which typically sense infection or cancer through the engagement of a clonotypic receptor, the activation of NK cells is regulated by signals received from a diverse array of both activating and inhibitory receptors. Since the cytotoxic response of NK cells requires recognition of host proteins, the majority of research has focussed on their response to either transformed or virus-infected cells. However, many bacteria also have the capacity to infect mammalian cells raising the potential that NK cells may impact their pathogenesis, particularly through the secretion of cytokines such as interferon-gamma.  This project aims to define the molecular mechanisms used by NK cells to sense bacterial infection and explore the potential of bacteria to subvert these processes. The Melbourne component of the project will assess how distinct intracellular bacterial infections stimulate or evade NK cell responses. The Brooks laboratory has expertise in NK cell receptor biology and has developed CRISPR/Cas9 -based methods to use gene editing to define the key mechanisms responsible for NK cell activation in diverse settings. The Schlee laboratory at Bonn University uses sophisticated approaches to define how cells sense foreign nucleic acids to better understand the nature of the very initial response to infection. Using these same models of bacterial infection, the Bonn arm of the project will define how these distinct infections interact with the diverse array of intracellular nucleic acid sensing receptors and then how this impacts crosstalk between the infected cell and NK cells. Understanding of the pathways by which bacterial infection modulates cross talk between infected cells and NK cells may lead to the identification of novel ways to enhance NK cell responses not only to bacteria but to viral infection and cancer as well as providing a pathway to develop therapeutic approaches to effectively manipulate the innate immune response. The first two years of project will be based in Melbourne before shifting to Bonn for a further 12 months.

Please visit the relevant links for more information on:

• Academic entry requirements
• Funding for Melbourne-based positions
• How to apply

The project focusses on the interaction between immune cells and Legionella pneumophila causing Legionnaire’s disease, an often-fatal form of pneumonia in which bacteria hijacking macrophage biology to form a replicative niche from where to establish infection. The project aims at identifying L. pneumophila factors that subvert macrophages using a multidisciplinary approach that includes whole-genome mutational screening, mRNAseq, metabolomics, proteomics, lipidomics, multicolour spectral flow cytometry and confocal microscopy. Research will be performed using cell lines and lung organoids in vitro as well as in preclinical animal models.

Please send a motivation letter, CV, two reference letters (or referee's names and contacts) and degree certificates with grades in one single pdf file using reference "IRTG" to Natalio Garbi (ngarbi@uni-bonn.de) by September 23^rd, 2022. 

Please visit the relevant links for more information on:

• Academic entry requirements
• Funding for Bonn-based positions
• How to apply

A major societal challenge over the last decades in the Western World and an important aspect of modern living is the reduced amount of physical movement combined with changes in dietary nutrition, leading to an increased incidence in chronic inflammation. Many inflammatory disorders manifest at barrier surfaces: allergies and asthma affect the lung, psoriasis affects the skin, while inflammatory bowel disease (IBD) results in chronic inflammation of the intestinal epithelium. Such inflammatory conditions are mainly driven by cytokine secretion of innate lymphoid cells (ILCs) and T helper cells. However, the etiology of these diseases is poorly understood, but is likely associated with changes in life-style coinciding with westernization, such as an overall increase in hygiene, abundant nutritional uptake, together with a reduced amount of physical activity. This project aims to unravel the effects of voluntary wheel running (VWR) in mice on the functionality of barrier immunology with particular focus on the regulation of metabolic pathways driving innate immune cell recruitment and T cell activation, differentiation and memory function. Based on exercise-induced changes in the host immune system we aim to elucidate to which extent a lack of exercise might on the one hand contribute to chronic inflammatory conditions (Crohn’s Disease, psoriasis or asthma), but also bacterial (Salmonella typhimurium) or viral (Influenza) infections. With our results we aim to assess whether exercise or an exercise-induced factor may be used as a potent therapeutic strategy in the future. The project will benefit from the complementary expertise of the Mackay lab in Melbourne (tissue resident T memory cells, bacterial and viral skin infection in in vivo models) and the Wilhelm lab in Bonn (dietary immunology, immunometabolism and barrier immunology).

Please visit the relevant links for more information on:

• Academic entry requirements
• Funding for Bonn-based positions
• How to apply

Regulatory T cells (Tregs) that express the transcription factor Foxp3 are critical to preserve immune homeostasis. They potently suppress self-reactive and inflammatory immune cells to prevent autoimmunity and tissue damage. However, in the context of cancer, they hinder protective immunosurveillance and anti-tumour immunity to promote tumour growth and metastasis. Given their essential role in immune homeostasis, innovations are needed to specifically target and neutralize Tregs in the tumour microenvironment without compromising self-tolerance.
Our project aims to discover the homeostatic mechanisms of tumour infiltrating/accumulating Tregs, using cutting-edge genomic technologies, novel pre-clinical models, flow cytometry and metabolic analyses. We also aim to explore the interaction between Tregs and tumours as well as tissues to explore potential molecular mechanisms that underpin checkpoint blockage failure in primary versus metastatic niches.

Please visit the relevant links for more information on:

• Academic entry requirements
• Funding for Bonn-based positions
• How to apply

The highly qualified candidate will work on the molecular mechanisms of chemokine gradient sensing of immune cells. Gradients of chemoattractants guide the recruitment of immune cells into organs, but it is incompletely understood how cells sense and respond to such stimuli. In recent years, we have engaged in setting up high-end microscopy- and microfluidics-based techniques to visualize and analyze migratory cell behavior quantitatively (Quast et al., Front Cell Dev Biol., 2022). The research project is designed to investigate cytoskeletal dynamics and intracellular events during navigation and turning behavior of motile immune cells. In the course of this, we will also use a CRISPR mutagenesis screen with direct in situ identification of functional hits.

Applicants should send their application documents in a single pdf file (max. 5 MB) including motivation letter, CV, scanned academic degrees, list of publications and the
contact details of two references. Successful candidates will begin on January 1, 2023 or later.
Please send your application by email until November 21, 2022 to irtg2168@uni-bonn.de.

Please visit the relevant links for more information on:

• Academic entry requirements
• Funding for Melbourne-based positions
• How to apply