Infection and Immunology

Main Research: Immunology and Infection

Term: 01.09.2018 – 28.02.2021, Extension maternity leave: 01.05.21-31.08.21

Disruption of immune homeostasis can impair antigen-specific responses and vaccine-induced immunity. Despite treatment, persistent inflammation in HIV deteriorates the immune system. This research project will investigate the effect of HIV on pre-existing vaccine-induced immunity. By means of polychromatic FACS and RNA-seq of antigen-specific T cells, we will dissect T cell responses to measles and tetanus; helping towards a needed rationale for immunization guidelines in HIV infected persons.

Principal Investigator Dr. Christiane Krystelle Nganou Makamdop Phone: +49 9131 85-26496 Email: ChristianeKrystelle.NganouMakamdop@uk-erlangen.de

Main Research: Immunology and Infection

Term: 16.10.2019 – 15.04.2022

The maintenance of healthy bone relies on a balance between bone formation by osteoblasts and bone resorption by osteoclasts. Recent findings indicate that the differentiation and function of osteoclasts can be regulated by certain changes in the cellular metabolism. Accordingly, we demonstrated that the metabolite itaconate inhibits osteoclastogenesis. The major aim of the presented project is the investigation of molecular mechanisms underlying this function of itaconate.

Principal Investigator Dr. Katerina Kachler phone: +49 9131 85-35907 e-mail: Katerina.Kachler@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.11.2019 – 30.04.2022

Rheumatoid arthritis is a common autoimmune disease. Anti-citrullinated-protein antibodies (ACPAs) have been identified as key players in RA . But a better understanding of the ACPA-producing B cells and of the transcriptional events in ACPA-specific B cells during the onset of RA is essential. Therefore, we plan to perform an in depth molecular characterization of the dynamic changes occurring inside the ACPA-specific B cell compartment during different phases of RA pathogenesis.

Principal Investigator Dr. René Pfeifle phone: +49 9131 85-29131 e-mail: Rene.Pfeifle@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.10.2019 – 31.03.2023

Ferroptosis is a recently identified type of programed necrotic cell death which is tightly regulated by GPX4. In this project the exact role of GPX4 and ferroptosis in myeloid cells under steady state conditions and during Salmonella Typhimurium infection will be investigated. GPX4-regulated ferroptotic cell death might display a new therapeutic target for treatment of acute infections in human patients.

Principal Investigator Dr. Barbara Ruder phone: +49 9131 85-35909 e-mail: Barbara.Ruder@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.09.19-28.02.2022

Obesity has become one of the leading global health concerns. Current research suggests a link between obesity, PD-L1 and the microbiome. This project will investigate the role of the microbiome on the function the regulation of adipose tissue T cell responses mediated by innate expression of PD-L1 in mice and humans. Using state-of-the-art RNA and 16S rRNA sequencing, flow cytometry and co-culture systems, we will reveal important mechanisms for the control of adipose tissue inflammation.

Principal Investigator Dr. Christian Schwartz phone: +49 9131 85-22650 e-mail: Christian.Schwartz@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.10.2020 – 31.11.2021

Ferroptosis is a novel form of regulated cell death with major importance in inflammatory conditions. The proposed study will elucidate the functional role of ferroptosis and its main regulator GPX4 in the lung under steady-state conditions and in the pathophysiology of the inflammatory lung disease of bronchial asthma. By characterizing the molecular pathways involved, we aim to lay the foundation for the development of new therapeutic avenues in the treatment of this frequent disease.

Principal Investigator Dr. Ingo Ganzleben phone: +49 9131 85-45161 e-mail: ingo.ganzleben@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.11.20 – 30.04.23.

Surface presentation of HLA class II-antigens can occur directly by the host cell or after intercellular transfer of the antigen to surrounding antigen presenting cells. We hypothesize that prior to surface presentation endogenously expressed class II-restricted antigens travel in different compartments as compared to exogenous antigens and therefore undergo differential processing. These processing steps which are critical for presentation, are characterized by antigen specific properties.

Principal Investigator Dr. Sascha Kretschmann phone: +49 9131 85-43162 e-mail: Sascha.Kretschmann@uk-erlangen.de

Main Research: Immunology and Infection

Term: 16.11.2020 – 15.05.2023

Intestinal fibrosis is a common complication in IBD and has limited therapeutic options. IL36R ligands are upregulated in CD and UC patients as well as CD patients with stenosis. The systemic blockade of IL36R signaling reduces intestinal inflammation and fibrosis in vivo. Deciphering the cell-type-specific roles of IL36 via the newly generated IL36Rfl/f mouse strain will help to understand the mode of action of a neutralizing IL36R antibody in humans.

Principal Investigator Dr. Kristina Scheibe phone: +49 9131 85-35892 e-mail: Kristina.Scheibe@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.01.2021 – 30.06.2023

We aim to investigate the composition of the gut virome as a marker for resistance against anti-TNF therapy in Crohn’s disease patients. We will functionally characterize the interaction of identified viruses with mucosal CD14+ macrophages. In particular, we will analyze mechanisms of increased mucosal IL23R expression and IL-23 production that mediate molecular resistance to anti-TNF therapy in Crohn’s disease, to finally elucidate a signaling pathway that determine non-response to therapy.

Principal Investigator Dr. Heike Knott phone: +49 9131 85-35131 e-mail: Heike.Schmitt@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.01.2021 – 30.06.2023

I could previously identify resident tissue macrophages (RTM) as anti-inflammatory protectors of stromal integrity. The molecular mechanisms that regulate this tissue-protective function, however, are unknown. My preliminary work strongly suggests that within stromal tissues exist extensive, heterocellular communication networks. I hypothesize that functional network communication between stromal fibroblasts and RTM coordinate biological behavior of tissues and facilitate RTM functionality.

Principal Investigator Dr. Stefan Uderhardt phone: +49 9131 85-45487 e-mail: Stefan.Uderhardt@uk-erlangen.de

Main Research: Immunology and Infection

Term: not started yet

A healthy skeleton relies on a balance between bone-forming osteoblasts and bone-resorbing osteoclasts. A shift towards increased osteoclast activity can therefore lead to bone loss. The immune system strongly affects osteoclast biology, usually promoting osteoclast development. Interestingly, we demonstrated that eosinophils negatively regulate osteoclast formation and activity. Thus, it is of high relevance to unveil the molecular mechanisms underlying this regulatory function of eosinophils.

Main Research: Immunology and Infection

Term: not started yet

Glucocorticoids are amongst the most important anti-inflammatory drugs, promoting inflammatory resolution via the functional reprogramming of macrophages, a process that promotes itaconate production. Though itaconate is an metabolite participating in immune-metabolic rewiring, its role and effects, as with the underlying mechanisms involved in its production, on immunometabolism and inflammatory resolution remain unknown, yet could contribute to further optimizing glucocorticoid treatment.