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Institute of Molecular Biology gGmbH and the International PhD Programme Mainz invite applications for a PhD project focusing on how interleukin-6 influences regulatory T cells during inflammation. The program offers a rich, international scientific community and training in advanced immunology techniques.
The successful candidate will work with state‑of‑the‑art facilities, including FACS, mouse models, and sequencing, while developing independent and collaborative research skills in a
Thinking of doing your PhD in the Life Sciences? The International PhD Programme (IPP) Mainz is offering talented scientists the chance to work on cutting edge research projects.
As an IPP PhD student, you will join a community of exceptional scientists working on diverse topics ranging from how organisms age or how our DNA is repaired, to how epigenetics regulates cellular identity or neural memory.
Tissue inflammation is often associated with increased levels of the pro-inflammatory cytokine interleukin-6 (IL-6), which can affect the function and stability of Foxp3⁺ Treg cells. How Treg cells survive and maintain their immunosuppressive function in an inflammatory environment remains poorly understood. Understanding the natural mechanisms that allow Treg cells to adapt to inflammation could help improve Treg cell-based therapies for inflammatory and autoimmune diseases.
IL-6 signaling is mediated by its biologically relevant receptor, IL-6R. Our preliminary data show that IL-6R is expressed on Treg cell precursors in the thymus and on naïve mature Treg cells, but is downregulated on Treg cells at sites of inflammation. Treg cells isolated from IL-6-deficient mice, which lack IL-6 signaling during development, exhibit poor survival in IL-6-driven inflammatory conditions. These findings suggest that IL-6 signaling during Treg cell development may help establish the properties required for mature Treg cells to survive and function in inflammatory environments.
We hypothesize that Treg cells dynamically adjust their response to IL-6 during development and in peripheral tissues, allowing them to maintain immune suppression during inflammation. This regulation may involve changes in IL-6R expression and associated transcriptional and epigenetic mechanisms.
In this project, we will investigate how IL-6 signaling shapes the function and fitness of Treg cells in inflamed tissues. We will use mouse models with cytokine overproduction or cytokine/receptor deficiency, as well as spontaneous and experimentally induced inflammatory models. Treg cell transfer experiments will be used to study their survival, stability, and suppressive function. We will combine multicolor flow cytometry (FACS), mouse immunology models, and sequencing approaches to identify the cellular and molecular mechanisms that control Treg cell fitness during inflammation.
The project is strongly immunological and will provide training in experimental mouse immunology, T-cell biology, flow cytometry, and molecular approaches.