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 within the open call on “Molecular Biomedicine & Ageing”. 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.
PhD Position: Immunology: Defining myeloid cell dynamics on a single-cell scale (m/f/d)
Activities and responsibilities
The research group of Johannes Mayer offers the following PhD project:
Circulating myeloid cells, which include monocytes, dendritic cells and granulocytes, are continuously replenished to maintain tissue homeostasis at steady state and have the capacity to rapidly reconfigure during local and systemic inflammation. Under non-inflammatory conditions, myelopoiesis follows relatively ordered differentiation routes that sustain circulating monocytes and granulocytes and seed tissue macrophage and dendritic cell compartments, with cell-cell communication cues from stromal, endothelial, and lymphoid niches helping to calibrate output and function. In contrast, inflammatory perturbations can shift both the composition and behavior of myeloid populations through altered cytokine landscapes, trafficking programs, and tissue-derived signals.
This reprogramming however does not only happen at the site of inflammation but also alters the bone marrow niche, affecting myelopoiesis, differentiation and stromal interaction, leading to emergency myelopoiesis or hematopoietic halt/shock. Using single-cell and multi-omic profiling integrated with trajectory inference and ligand-receptor/network modeling, the project will map how inflammatory signals reroute progenitor-to-effector differentiation, expand specific myeloid subsets, and reshape functional programs. It will test the concept that inflammation induces not only accelerated “emergency” output but can also produce phases of progenitor dysfunction or suppression-where stem/progenitor compartments enter protective quiescence, exhaustion, or shock-like states-resulting in delayed or maladaptive reconstitution.
PhD Project: Defining Myeloid cell Ageing and its immunological impact on a single cell level
In our lab, we have established an integrated toolkit to study myeloid biology at single-cell resolution, combining single-cell sequencing with large, high-dimensional flow cytometry panels and a suite of transgenic mouse lines. In addition we utilize well-characterized inflammatory models that span both systemic and local inflammation, enabling us to track myeloid populations across compartments and over time with high phenotypic and molecular precision.
Building on these resources, this project aims to profile myeloid cell dynamics, poiesis, and the myeloid interactome in bone marrow and peripheral tissues at steady state and under local versus systemic inflammation to define changes in myeloid cell output and reprogramming leading to functional consequences for comorbidities and ageing-related immune dysfunction.
This PhD requires a strong background in immunology, previous experience with complex phenotyping of immune cells via single-cell sequencing including sequencing library preparation, bioinformatics and a willingness to work with in vivo animal models, including handling, experimental design and tissue processing and analysis.
If you are interested in this project, please select Mayer (Dynamics) as your group preference in the IPP application platform.
Circulating myeloid cells, which include monocytes, dendritic cells and granulocytes, are continuously replenished to maintain tissue homeostasis at steady state and have the capacity to rapidly reconfigure during local and systemic inflammation. Under non-inflammatory conditions, myelopoiesis follows relatively ordered differentiation routes that sustain circulating monocytes and granulocytes and seed tissue macrophage and dendritic cell compartments, with cell-cell communication cues from stromal, endothelial, and lymphoid niches helping to calibrate output and function. In contrast, inflammatory perturbations can shift both the composition and behavior of myeloid populations through altered cytokine landscapes, trafficking programs, and tissue-derived signals.
This reprogramming however does not only happen at the site of inflammation but also alters the bone marrow niche, affecting myelopoiesis, differentiation and stromal interaction, leading to emergency myelopoiesis or hematopoietic halt/shock. Using single-cell and multi-omic profiling integrated with trajectory inference and ligand-receptor/network modeling, the project will map how inflammatory signals reroute progenitor-to-effector differentiation, expand specific myeloid subsets, and reshape functional programs. It will test the concept that inflammation induces not only accelerated “emergency” output but can also produce phases of progenitor dysfunction or suppression-where stem/progenitor compartments enter protective quiescence, exhaustion, or shock-like states-resulting in delayed or maladaptive reconstitution.
PhD Project: Defining Myeloid cell Ageing and its immunological impact on a single cell level
In our lab, we have established an integrated toolkit to study myeloid biology at single-cell resolution, combining single-cell sequencing with large, high-dimensional flow cytometry panels and a suite of transgenic mouse lines. In addition we utilize well-characterized inflammatory models that span both systemic and local inflammation, enabling us to track myeloid populations across compartments and over time with high phenotypic and molecular precision.
Building on these resources, this project aims to profile myeloid cell dynamics, poiesis, and the myeloid interactome in bone marrow and peripheral tissues at steady state and under local versus systemic inflammation to define changes in myeloid cell output and reprogramming leading to functional consequences for comorbidities and ageing-related immune dysfunction.
This PhD requires a strong background in immunology, previous experience with complex phenotyping of immune cells via single-cell sequencing including sequencing library preparation, bioinformatics and a willingness to work with in vivo animal models, including handling, experimental design and tissue processing and analysis.
If you are interested in this project, please select Mayer (Dynamics) as your group preference in the IPP application platform.
Qualification profile
Are you an ambitious scientist looking to push the boundaries of research while interacting with colleagues from multiple disciplines and cultures? Then joining the IPP is your opportunity to give your scientific career a flying start!
All you need is:
All you need is:
- Master or equivalent
- Interactive personality & good command of English
- 2 letters of reference
We offer
We offer
For more details on the projects offered and how to apply via the online form using the apply button.
The deadline for applications is 1 April 2026. Interviews will take place at IMB in Mainz on 22 & 23 June 2026.
Starting date: 1 July - 31 December 2026
- Exciting, interdisciplinary projects in a lively international environment, with English as our working language
- Advanced training in scientific techniques and professional skills
- Access to our state-of-the-art Core Facilities and their technical expertise
- Fully funded positions with financing until the completion of your thesis
- A lively community of more than 200 PhD students from 44 different countries
For more details on the projects offered and how to apply via the online form using the apply button.
The deadline for applications is 1 April 2026. Interviews will take place at IMB in Mainz on 22 & 23 June 2026.
Starting date: 1 July - 31 December 2026
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