Infection and Immunology

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 (bonus time until 15.11.2023)

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: 01.01.2022 – 30.06.2024

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.

Principal Investigator Dr. Darja Andreev Phone: +49 9131 85-29291 Email: darja.andreev@uk-erlangen.de

Main Research: Immunology and Infection

Term: 01.01.2022 – 30.06.2024

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.

Principal Investigator Dr. Jean-Philippe Auger Phone: 09131 85-39313 Email: Philippe.Auger@extern.uk-erlangen.de