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Immunology and Infection

Term: 01.07.2016 – 30.06.2019

Tumor necrosis factor (TNF)-deficient mice fail to control the intracellular protozoan pathogen Leishmania major, despite an intact IFN-γ (Th1) immune response and a sustained expression of type 2 nitric oxide synthase (NOS2) mRNA and protein, which is the key antileishmanial effector pathway. Here, we will test the hypothesis that TNF conveys protection by alternative mechanisms including the induction of NOS2 cofactors and the downregulation of arginine-metabolizing enzymes such as arginase 1.

Principal Investigator
Prof. Dr. Christian Bogdan
phone: +49 9131 85-22551
e-mail: christian.bogdan@uk-erlangen.de

Term: 01.07.2016 – 30.06.2019

We propose a systematic, unbiased approach at identifying cellular restriction factors of DNA viruses using the powerful CRISPR/Cas9 knockout technology, through a lentiviral sgRNA library targeting each human gene with several independent constructs. Our focus is on cellular factors that restrict or promote the replication of Herpesviruses and/or limit the growth of tumor cells transformed by KSHV and EBV. These factors represent primary therapeutic targets.

Principal Investigator
Prof. Dr. Armin Ensser
phone: +49 9131 85-22104
e-mail: armin.ensser@fau.de

Term: 16.06.2016 – 15.06.2019

Preliminary data show a central role of the IL-23/Th17 axis during the control of autoantibody activity during rheumatoid arthritis (RA). During  the proposed project, we aim to elucidate underlying molecular mechanisms and evaluate their relevance in patients suffering from RA.

Principal Investigator
Prof. Dr. Gerhard Krönke
phone: +49 9131 85-33015
DECT: 09131 85-43012
e-mail: gerhard.kroenke@uk-erlangen.de
Principal Investigator
Prof. Dr. Falk Nimmerjahn
phone: +49 9131 85-25050e-mail: falk.nimmerjahn@fau.de

Term: 01.07.2016 – 30.06.2019

The DNA-damage response (DDR) requires the kinase ATM and is essential for the integrity of the host genome. We observed activation of the ATM kinase pathway in Toll-like receptor (TLR)-stimulated macrophages and a modulation of the inflammatory response by ATM-inhibition. We propose now detailed studies to elucidate  the molecular mechanisms and the consequences of ATM/DDR activation for the host response, protection and immunopathology during infection.

Principal Investigator
Prof. Dr. Roland Lang
phone: +49 9131 85-22979
DECT: 09131 85-46904
e-mail: roland.lang@uk-erlangen.de

Term: 01.07.2016 – 30.06.2019
We could show that certain deubiquitinating enzymes (DUBs) play an essential role in HIV-1 replication, at least by regulating Gag processing, virus infectivity, and entry of Gag into the MHC-I pathway. DUB-inhibitors offer a new way for antiretroviral therapy as they (1) target genetically stable cellular factors, (2) interfere with virus spread, and (3) have the potential to improve immune recognition of HIV-1+-cells. 
Principal Investigator
Prof. Dr. Ulrich Schubert
phone: +49 9131 85-26478
e-mail: ulrich.schubert@viro.med.uni-erlangen.de

Term: 01.07.2016 – 30.06.2019

The aim of this project is to elucidate the function of CD83 expressed on Tregs. Recently we reported that after activation Tregs rapidly upregulate CD83 expression, providing a new phenotypic marker for activated Tregs. However, the functional importance of this expression is completely unknown. Using our recently generated conditional KO animals, whereby CD83 expression is exclusively deleted on Tregs we aim to elucidated the role of CD83 for activation and suppressive capacity of Tregs.

 
Principal Investigator
Prof. Dr. Alexander Steinkasserer, PhD
phone: +49 9131 85-36725
e-mail: alexander.steinkasserer@uk-erlangen.de

Term: 01.07.2016 – 30.09.2019
Checkpoint inhibitors (CPI) show great promise in improving immune control of tumors. However, the co-inhibitory receptors targeted by CPIs also play an important role during the induction of immune responses by viral vaccines. Therefore the aims of the project are to better understand the consequences of CPI therapy on vaccine-induced adaptive immune responses and to explore the potential of CPIs as a systemic and local immunomodulatory vaccine adjuvant.
Principal Investigator
Prof. Dr. Klaus Überla
phone: +49 9131 85-23563
Fax: 09131 85-22101
e-mail: klaus.ueberla@fau.de

Term: 01.07.2016 – 30.06.2019

Although cell death is of fundamental importance in almost all hepatic diseases such as autoimmune hepatitis , there is still no precise knowledge about the underlying mechanisms.  The aim of this proposal is to elucidate the role of MLKL-dependent programmed cell death in the pathogenesis of liver diseases.

Principal Investigator
PD Dr. Stefan Wirtz
phone: +49 9131 85-35882
e-mail: stefan.wirtz@uk-erlangen.de
Principal Investigator
Dr. Claudia Günther
phone: +49 9131 85-35909
e-mail: c.guenther@uk-erlangen.de