Term: 01.07.2023 – 31.12.2026
New medications for the treatment of chronic wounds are urgently needed. Our preliminary data show that sCD83 accelerated wound healing processes in a systemic as well as a topical treatment. Cellular analyses revealed the increase of pro-resolving macrophages, known to improve wound healing processes. These striking regenerative capacities make scD83 a promising candidate to treat chronic- and hard-to-heal wounds. Within the current project we aim to elucidate the underlying mechanisms.
Term: not started yet
We will define the relevance of VRAC for T cell function in colitis and validate VRAC as a potential target for IBD therapy. Our initial data point to a functional role of VRAC in T cell-driven colitis and implicate that VRAC modulates immunometabolism and mechanical properties of T cells. Using VRAC KO mice and IBD tissue samples, we will elucidate the colitis-regulating capacity of VRAC in T cells, identify modulators of VRAC expression and define its interplay with T cell immunometabolism.
- PD Dr. Imke Atreya, imke.atreya@uk-erlangen.de
Term: not started yet
Primary Sjögren’s syndrome (PSS) is an autoimmune disease causing chronic inflammation of exocrine glands, dry mouth and eyes. Our preliminary data identify RIP kinases as novel regulators of salivary gland homeostasis and potential factors in PSS. Inducible RIP kinase-deficient mice develop PSS-like disease and implicate this kinase in immune regulation and epithelial homeostasis within the salivary gland. This proposal aims to clarify the role of RIP kinases in the salivary gland and in PSS.
Term: 01.06.2026 – 30.11.2028
This project investigates the role of estrogen receptor (ER) signaling in B cell activation and metabolic reprogramming in male and female mice. Since women have a higher incidence of autoimmune diseases like rheumatoid arthritis, the impact of ERα and ERβ on B cell proliferation, antibody class switching, and arthritis development is analyzed. Using RNA sequencing, flow cytometry, and metabolic assays, the study aims to uncover sex-specific differences and potential therapeutic targets.
Term: 01.04.2026 – 30.09.2028
Amino acids such as arginine and proline influence the immune system as well as different microbial organisms. However, the influence of both amino acids on immune defense and microbiota-mediated colonization resistance or on Salmonella virulence is unknown. Therefore, we will characterize a) the influence of arginine-dependent microbiota on Salmonella infections and b) the role of proline in Salmonella virulence and anti-bacterial immune response.
Term: 01.02.2026 – 30.10.2028
We found in mice and humans a plasma cell population with high surface sialylation. We hypothesize that this population represents activated plasma cells that experience ER stress and await survival signals. We will characterize these cells in mice and humans regarding ER stress, survival, signalling and metabolism, analyse plasma cells from mice with B cell intrinsic elevated ER stress, investigate niche support and how surface sialylation influences plasmablast/ plasma cell fate.
Term: 01.01.2026 – 30.06.2028
Intestinal B cells, including plasmablasts are potentially involved in the pathogenesis of ulcerative colitis (UC), as their elevated mucosal presence has recently been described in resistant disease courses. Based on own findings of a successful CD19 CAR T cell treatment in a patient with refractory UC, we aim to characterize the role of gut B cells in perpetuating the inflammatory process and to understand the therapeutic potential of depleting specific B cell subsets in UC.
Term: Not started yet
Allergic asthma (AA) is an inflammatory lung disease. At present it is unclear how macrophage populations in the lung are altered at different stages of allergic inflammation (onset, acute phase, resolution). We will use a mouse AA model to address the population dynamics of macrophages using fate mapping mice, interrogate the role of IL-4/IL-13 and activating or inhibitory Fc receptors, and study the impact of macrophages on their tissue environment with mouse and human lung organoids.
Term: 01.06.2026 – 30.11.2028
T cells are a main driver of inflammatory bowel disease, but the dynamics of their trafficking to and from the gut are incompletely understood. Our project combines unique trafficking models with innovative mathematical approaches to determine and manipulate the kinetics of T cell trafficking in chronic intestinal inflammation. In the long-term perspective, this might lead to improved therapeutic strategies in IBD.