Topics

Sub Project 1: Impact of chronic hepatitis on DC/T cell functions in viral infections

Chronic inflammation negatively affects systemic anti-viral host defense and the clearance of bacterial and viral infections. In this project we aim to unravel the impact of chronic liver inflammation on the anti-viral immune responses using LCMV and influenza A virus (IAV) infection models.

Dr. Zeinab Abdullah

Institute of Experimental Immunulogy
zeinab.abdullah(at)ukbonn.de

 

 

Lisa Assmus
PhD Student

Institute of Experimental Immunulogy
s6liassm(at)uni-bonn.de

Nicole La Gruta

Dept. of Microbiology and Immunulogy
nicole.la.gruta(at)monash.edu

Sub Project 2: Increasing Plasmodium immunogenicity to induce protective CTL immunity against Malaria

Malaria infection is still a major cause of childhood mortatility, which underlines the medical need for a protective vaccine. Vaccination using large numbers of attenuated Sporozoites (SPZ) is in principle able to induce protective tissue resident memory T-cells (TRM) against liver stage malaria, but it is impractical for routine use. In this project we evaluate whether novel vaccine adjuvants that selectively engage nucleic acid sensors of the innate immune system improve the robustness and persistence of the TRM response, while allowing a dose sparing use of attenuated SPZ.

Winfried Barchet

Inst. of Clinical Chemistry & Clinical Pharmacology
winfried.barchet(at)ukbonn.de

Ana Maria Valencia Hernandez
PhD Student

Inst. of Clinical Chemistry & Clinical Pharmacology
ana.valencia(at)uni-bonn.de

William R. Heath

Dept. of Microbiology and Immunology
wrheath(at)unimelb.edu.au

Matthias Enders
PhD Student

Dept. of Microbiology and Immunology
menders(at)student.unimelb.edu.au

Sub Project 3: Influence of intestinal migratory DCs on immunity against Salmonella

The chemokines CCL17 and CCL22 promote T cell/dendritic cell interactions during the induction of adaptive immune responses. CCL17 has been associated with the pathogenesis of allergic and inflammatory diseases, whereas CCL22 appears to rather play an immunosuppressive role. Using a mouse model for invasive Salmonellosis and specific knockout mice for both chemokines, we study the influence of CCL17 and CCL22 on the immune responses against Salmonella enterica serovar Typhimurium after oral infection. We are analyzing the myeloid cell populations responsible for transporting bacteria from the gut to mesenteric lymph nodes and investigate the importance of the chemokines for the induction of antigen-specific CD4 T cell responses in the context of vaccination. This analysis is further facilitated by the development of novel MHC class II tetramers for detection of Salmonella-specific T cells.

Irmgard Förster

Life & Medical Sciences Institute
irmgard.foerster(at)uni-bonn.de

Ana-Belen Erazo
PhD Student

Life & Medical Sciences Institute
anna_erazo(at)gmx.de

Richard A. Strugnell

Dept. of Microbiology and Immunology
rastru(at)unimelb.edu.au                   

John Hamilton

Dept. of Medicine, Royal Melbourne Hospital
jahami(at)unimelb.edu.au

Adrian Semeniuk
PhD Student

Dept. of Microbiology and Immunology
asemeniuk(at)student.unimelb.edu.au

Sub Project 4: Interplay between myeloid and T cells for anti-bacterial lung immunity

Legionella spp may cause a serious type of bacterial pneumonia called Legionnaire's disease and thus, pose a significant health risk in man. In collaboration with Prof. van Driel, University of Melbourne, we are investigating the cellular and molecular mechanisms governing host immune responses against Legionella. Using molecular, immunological, microbiological and imaging techniques, we are investigating (1) myeloid cells that are permissive for Legionella infection and replication; (2) the role of inflammasome activation in defence against Legionella by using genetically-modified mouse models and visualization of inflammasome activation, (3) molecular pathways in myeloid cells induced by Legionella infection, and (4) the contribution of lymphoid cells in the defence against Legionella. These studies will highlight key mechanisms controlling Legionella replication and may contribute towards new therapeutic strategies for pulmonary infections.

Natalio Garbi

Institute of Experimental Immunology
ngarbi(at)uni-bonn.de

Victoria Scheiding
PhD Student

Institute of Experimental Immunology
vscheidi(at)uni-bonn.de

Ian van Driel

Dept. of Microbiology and Immunology
i.vandriel(at)unimelb.edu.au

Markus Johannes Fleischmann

Dept. of Microbiology and Immunology
markus.fleischmann92(at)gmx.de

Sub Project 5: Functional consequences of integration of viral and bacterial immune sensing signals

Gunther Hartmann

Institute of Clinical Chemistry & Clinical Pharmacology
gunther.hartmann(at)uni-bonn.de

Michaela Bergmann
PhD Student

Institute of Clinical Chemistry & Clinical Pharmacology
mbergmann(at)uni-bonn.de

Patrick Reading

Dept. of Microbiology and Immunology
preading(at)unimelb.edu.au

Lara Schwab

Dept. of Microbiology and Immunology
Lara.Schwab(at)gmx.de

Sub Project 6: Role of XCL1 on DC migration in actuate viral infections

XCL1 is a chemokine that is expressed by NK cells and CD8 T cells upon activation. The receptor for XCL1 is called XCR1 and is exclusively expressed on a subset of Dendritic cells. In this project we address the role of the XCL1-XCR1 axis in the context of acute viral infections.

Wolfgang Kastenmüller

Institute of Experimental Immunology
wkastenm(at)uni-bonn.de

Sabrina Dähling
PhD Student

Institute of Experimental Immunology
sdaehl(at)uni-bonn.de                  

Sammy Bedoui

Dept. of Microbiology and Immunology
sbedoui(at)unimelb.edu.au

Elise Gressier
PhD Student

Dept. of Microbiology and Immunology
egressier(at)unimeldb.edu.au

Sub Project 7: Control of immunity against Legionella pneumophila by Arf-GTPase exchange factors

Cytohesins are guanine nucleotide exchange factor for ARF-GTPases which regulate important aspects of vesicle transport in cells, but are also involved in the signal transduction of important cell surface receptors, e.g. integrins and the insulin receptor. In the course of this project we will employ knock-out models for the cytohesins to unravel their roles in the innate immune response againt bacteria such as legionella, which reside in intracellular, vesicular compartments.

Waldemar Kolanus

Life & Medical Sciences Institute
wkolanus(at)uni-bonn.de

Anastasia Solomatina
PhD Student

Life & Medical Sciences Institute
anastasia.solomatina(at)uni-bonn.de                  

Elisabeth Hartland

Dept. of Microbiology and Immunology
hartland(at)unimelb.edu.au

Linda Rafeld
PhD Student

Dept. of Microbiology and Immunology
hrafeld@student.unimelb.edu.au

Sub Project 8: Improving cross-presentation and vaccination by harnessing MAIT cells

Our joint project aims at harnessing a recently discovered immune cell type, the mucosa-associated invariant T (MAIT) cells, to improve vaccination strategies against mucosal virus infections. It combines the expertise of Christian Kurts on antigen cross-presentation with that of Dale Godfrey on innate lymphocyte subsets. The PhD project encompasses basic scientific questions regarding immune regulation, immune cell migration and cell biology and translational question in human immunology. 

Christian Kurts

Institute of Experimental Immunology
ckurts(at)uni-bonn.de

Marie-Sophie Philipp
PhD Student

Institute of Experimental Immunology
msphil(at)uni-bonn.de 

Dale Godfrey

Dept. of Microbiology and Immunology
godfrey(at)unimelb.edu.au

Marc Rigau
PhD Student

Dept. of Microbiology and Immunology
mrigau@student.unimelb.edu.au

Sub Project 9: Systems analysis of paracrine effects after inflammasome activation

Eicke Latz

Institute of Innate Immunity
eicke.latz(at)uni-bonn.de

Christina Budden
PhD Student

Institute of Innate Immunity
s6chbudd(at)uni-bonn.de                        

Paul Hertzog

Monash Institute of Medical Research
paul.hertzog(at)hudson.org.au

Sarah Straub
PhD Student

Dept. of Microbiology and Immunology
sstraub(at)student.unimelb.edu.au

Sub Project 10: Molecular regulation of suppressive lymphocytes and myeloid cells in non-lymphoid tissues

In order to avoid complete organ destruction, it is important to understand immune-suppressive mechanisms that arise in non-lymphoid tissues during acute and chronic inflammation. Such immune regulation can stem from suppressive lymphocyte populations such as regulatory T cells or myeloid cell subsets (e.g. DC or MDSCs). In this project we are analyzing and identifying the molecular regulators that control the transcriptional and metabolic profiles of these suppressive immune populations in the inflamed tissues of kidney, lung and skin.

Isis Ludwig-Portugall

Institute of Experimental Immunology
isis.ludwig-portugall(at)ukbonn.de

Sebastian Liene
PhD Student

Institute of Experimental Immunology
s.liene(at)uni-bonn.de

Axel Kallies

Walter & Eliza Hall Institute of Medical Research
kallies(at)wehi.edu.au

Santiago Valle Torres

Walter & Eliza Hall Institute of Medical Research
svalletorres(at)student.unimelb.edu.au

Sub Project 11: Cell-to-cell communication within the immune system studied in humans

This project aims to unravel novel pathways and mechanisms of cell-cell communication in immunological complex tissues by single-cell RNA sequencing and computational modelling. These interaction models will be tested in a murine influenza model.

Joachim L. Schultze

Life & Medical Sciences Institute
j.schultze(at)uni-bonn.de

Patrick Günther
PhD Student

Life & Medical Sciences Institute
s6paguen(at)uni-bonn.de

Stephen J. Turner

Dept. of Microbiology and Immunology
stephen.j.turner(at)monash.edu

Vibha Udupa

Dept. of Microbiology and Immunology
vibhaudupa19(at)gmail.com

Sub Project 12: Tissue-resident cytotoxic T memory cells in skin melanoma

Malignant melanoma is highly aggressive skin cancer and a paradigm disease for the development of novel immunotherapeutic strategies. In this project we aim to determine the role of permanently tissue–resident cytotoxic T memory (TRM) cells in melanoma growth surveillance. We also analyze the reciprocal interactions between melanoma cells and melanoma–specific TRM cells. The findings will improve our understanding how melanoma cells and the immune system could be re-educated to improve current treatments.

Michael Hoelzel

Inst. of Clinical Chemistry & Clinical Pharmacology
mhoelzel(at)uni-bonn.de

Maike Effern
PhD Student

Inst. of Clinical Chemistry & Clinical Pharmacology
maike.effern(at)ukbonn.de

Thomas Gebhardt

Dept. of Microbiology and Immunology
gebhardt(at)unimelb.edu.au

Emma Bawden
PhD Student

Dept. of Microbiology and Immunology
emma.bawden(at)student.unimelb.edu.au

Sub Project 13: Cell biology of Alzheimer´s disease; Ab production and the neuroinflammation

Aim of this project is to investigate the influence of neuroinflammation on amyloid beta production, the impact of immunostimulated microglia supernatants on BACE1 and APP trafficking and amyloid beta production in primary neurons.

Michael Heneka

Departement of Neurology, Clinical Neurosciences Unit
michael.heneka(at)ukbonn.de

Alessa Webers
PhD Student

Department of Neurology, Clinical Neurosciences Unit
alessa.webers(at)ukb.uni-bonn.de

Paul Gleeson

Dept. of Biochemistry and Molecular
paul.gleeson(at)unimelb.edu.au

Andreas Pannek

Dept. of Biochemistry and Molecular
apannek(at)student.unimelb.edu.au

Sub Project 14: Post-transcriptional regulation of the NLRP3 inflammasome

NLRP1 was the first NLR protein described to form an inflammasome, recruiting ASC to activate Caspase-1, which processes interleukin-1β and interleukin-18. In this joined project, we aim at defining the genetic and structural information that regulates this innate immune sensor. Autolytic cleavage within the FIIND domain of NLRP1 has been implicated in activation, and common variants near this region are susceptibility loci for a broad range of autoimmune diseases. The familial loss of function mutations in the N-terminal pyrin domain highlight that this autolytic cleavage is indeed a pre-requisite for NLRP1 activation, liberating a C-terminal fragment containing a CARD domain to form an ASC dependent inflammasome. We want to determine the structural and functional basis of this NLRP1 regulation mechanisms.

Matthias Geyer

Institute of Innate Immunity
matthias.geyer(at)caesar.de

Jonas Möcking
PhD Student

Institute of Innate Immunity
j.moecking(at)gmail.com     

Seth Masters

Walter & Eliza Hall Institute of Medical Research
masters(at)wehi.edu.au

Annemarie Steiner

Walter & Eliza Hall Institute of Medical Research
annemarie_steiner(at)gmx.de

Sub Project 15: Nucleic acid sensing by T cells during HIV-1 infection

The aim of the project is to evaluate nucleic acid recognition based signaling pathways in resting or activated T cells and if presence of HIV-1 impair or mutate such pathways of the innate immune system in persistently infected T cells. 

Martin Schlee

Institute of Clinical Chemistry & Clinical Pharmacologie
martin.schlee(at)caesar.de

Marvin Holz
PhD Student

Institute of Clinical Chemistry & Clinical Pharmacologie
marvin.holz(at)hhu.de   

Damian Francis John Purcell

Dept. of Microbiology and Immunology
dfjp(at)unimelb.edu.au

Sharon Lewin

Dept. of Biochemistry and Molecular Biology
sharon.lewin(at)unimelb.edu.au

Abdalla Ali
PhD Student

Dept. of Microbiology and Immunology
abdallaa(at)student.unimelb.edu.au

Associated Projects

Inflammasomes in Intestinal Epithelial Cells

Inflammasomes are macromolecular signaling complexes that integrate information on signs of cell damage or infection and coordinate immune responses. While the role and some mechanistic details of inflammasome assembly in myeloid cells are well understood, it is now clear that additional cell types are able to assemble inflammasomes in response to pathogen or danger-associated molecular patterns. We will investigate the role and cell biology of inflammasome assembly in intestinal epithelial cells (IECs) cultivated in 3D intestinal organoids. Using novel biomarkers for inflammasome assembly and reporters for IFN-β expression, we will determine which IEC cell types assemble inflammasomes in response to virus infection, which sensors are involved, and how responses are coordinated between different cell types and signaling pathways.

Florian Schmidt

Institute of Innate Immunity
fschmidt(at)uni-bonn.de

Florian Gohr

Institute of Innate Immunity
florian.gohr(at)uni-bonn.de

Jason Mackenzie

Dept. of Microbiology and Immunology
Jason.mackenzie(at)unimelb.edu.au

 

Alice Trenerry

Dept. of Microbiology and Immunology
alice.trenerry(at)uq.net.au

The function of lipid metabolism in the maintenance of type 2 immune responses

Survival of the host relies on the establishment of a functional barrier immune defense that must be maintained in fluctuating states of food availability. Innate lymphoid cells type 2 (ILC2) are an important component of tissue immunity involved in the maintenance and repair of tissue barriers such as the lung and intestine. However, chronic activation of ILC2 may result in immune pathology and asthma. We are interested in unraveling whether and how lipid metabolism induced by different metabolic restrains dictates the development of protective versus pathogenic ILC2 responses.

Christoph Wilhelm

Institute of Clinical Chemistry & Clinical Pharmacologie
christoph.wilhelm(at)uni-bonn.de

 

Marcel Michla

Institute of Clinical Chemistry & Clinical Pharmacologie
mmichla(at)uni-bonn.de

Laura Mackay

Dept. of Microbiology and Immunology
lkmackay(at)unimelb.edu.au