Infection and Immunology
Main Research: Immunology and Infection
Term: 01.11.2023 – 30.04.2026
T cells play a key role in IBD, but the impact of Stat5 in CD4+ T cells for chronic colitis is unclear so far. Based on preliminary data demonstrating spontaneous chronic colitis in conditional Stat5 KO mice and decreased Stat5 expression in IBD, I hypothesize that Stat5 in CD4+ T cells counteracts colitis. Thus, in this project, I will explore the mechanisms and effects of CD4-specific Stat5 signalling for experimental colitis and IBD, aiming to identify novel approaches for future therapy.
Dr. Tanja Müller
Medizinische Klinik 1
- E-Mail: tanja.mueller@uk-erlangen.de
Main Research: Immunology and Infection
Term: 01.10.2023 – 31.03.2026
The secretion of correctly glycosylated protective antibodies by long-lived plasma cells is essential for our immune protection. To survive and produce antibodies, long-lived plasma cells require an optimized metabolism. The aim of this study is to determine whether the glucose transporter GLUT1 plays a role in the metabolism of long-lived plasma cells and the functionality of their antibodies. Therefore, we will study a GLUT1-deficient mouse model and patients with GLUT1-deficiency syndrome.
Dr. Katharina Pracht
Molekular-Immunologische Abteilung
- E-Mail: katharina.pracht@uk-erlangen.de
Main Research: Immunology and Infection
Term: 01.09.2023 – 28.02.2026
To date, it is still obscure why in some patients with psoriasis the autoimmune process is restrained to the skin, whereas in other it extends to the joints. We will adopt models resembling psoriasis and psoriatic arthritis, with the aim of studying the joint involvement secondary to skin inflammation. The comprehension and characterization of the underlying mechanisms involved in the “skin-joint axis” is pivotal for a better understanding of the link between physical barriers and autoimmunity.
Dr. Maria Gabriella Raimondo
Medizinische Klinik 3
Main Research: Immunology and Infection
Term: 01.01.2024 – 31.08.2026
PU.1 controls the transcriptional network of matrix production in fibrotic fibroblasts. We have now found that PU.1 is also expressed in matrix-producing osteoblasts. In this proposal, we aim to study the PU.1 network in biopsies from patients with osteoproliferative arthritis by imaging mass cytometry, to dissect PU.1-driven transcription in human osteoblastogenic cultures by ATTAC/CHIP/RNA-seq, and to use a novel osteoblast-targeting PU.1 inhibitor in experimental osteoproliferative arthritis.
Dr. Simon Rauber
Medizinische Klinik 3
- E-Mail: simon.rauber@uk-erlangen.de
Main Research: Immunology and Infection
Term: 01.01.2024 – 30.06.2026
This project aims at identifying the expression of the CFTR complex and functionally characterising its role in in peripheral blood mononuclear cells in the context of Cystic Fibrosis (CF). Moreover, the effects of a CFTR-modulating therapy with Elexacaftor – Tezacaftor – Ivacaftor (ETI) on immune cell function and regulation will be examined in a CFTR knock-out cell line and a CF pig model as well as primary patient-derived cells.
Schwerpunkt: Infektionsforschung und Immunologie
Term: 01.11.2024 – 30.04.2027
Various factors contribute to the pathogenesis of ulcerative colitis (UC). Importantly, telomere shortening is often observed in intestinal epithelial cells (IECs) of patients with UC. Nevertheless, the functional role telomere length in IECs is poorly understood. This project aims to evaluate how telomere length is involved in the regulation of pro-inflammatory pathways and affects the barrier integrity in patients with UC.
Dr. Oana-Maria Thoma
Medizinische Klinik 1
- E-Mail: oana-maria.thoma@uk-erlangen.de