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 Hallmarks of Myeloid cell ageing on a single cell level (m/f/d)
Activities and responsibilities
The research group of Johannes Mayer offers the following PhD project:
Myeloid cells, which include monocytes, macrophages, dendritic cells, and granulocytes, sit at the frontline of immune defense and tissue homeostasis, yet they are also among the immune compartments most visibly remodeled by ageing. These changes are influenced by several hallmarks of ageing and a central aim will be to disentangle intrinsic (cell-autonomous) from extrinsic (environment-driven) hallmarks of ageing and determine how they reshapes myeloid biology. Intrinsically, accumulated DNA damage, epigenetic drift, telomere attrition, mitochondrial dysfunction, impaired proteostasis/autophagy, and heightened cellular senescence programs can bias myeloid differentiation and survival, rewire metabolic set-points, and “pre-tune” signaling thresholds, leading to exaggerated inflammatory outputs or blunted immunological functions. Extrinsically, the ageing tissue environment shows chronic low-grade inflammation, altered cytokine and growth-factor availability, changes in stromal and endothelial cues, shifts in the microbiome and barrier integrity, and increased exposure to senescence-associated secretory phenotypes (SASP) can continuously imprint new activation states on myeloid cells, driving maladaptive inflammation, defective tissue-repair polarization, and compromised antigen presentation.
Together, these intrinsic and extrinsic changes coincide with age-associated shifts in hematopoiesis and a rising inflammatory baseline (“inflammageing”), yielding myeloid populations with altered pattern-recognition signaling, cytokine production, metabolic profiling and migratory behavior. These changes are highly relevant and linked to poorer vaccine responses, increased infection risk, chronic inflammatory pathology, and impaired tissue repair, yet the field still lacks a precise, cell-type-resolved definition of “myeloid ageing”.
PhD project: Defining Myeloid cell Ageing and its immunological impact on a single cell level
In our lab we have developed a number of tools to study myeloid cells on a single cell level. This includes single-cell RNAseq and large high-dimensional flow cytometry panels and a collection of transgenic mouse models specifically engineered for the reporting, lineage tracing, or conditional deletion of defined dendritic cell subsets. In this project the aim is to profile the tissue-specific myeloid cell single-cell landscape of young and old mice, establish tissue-specific murine models of premature ageing, define myeloid population specific SASP and mitochondrial signatures and thus unravel cell-intrinsic and extrinsic hallmarks of myeloid cell ageing.
This PhD requires a strong background in immunology, previous experience with the complex phenotyping of immune cells on a single-cell level and proficiency in working with in vivo animal models, including handling, experimental design and tissue processing and analysis. Experience in bioinformatics is a plus.
If you are interested in this project, please select Mayer (Ageing) as your project preference in the IPP application platform.
Myeloid cells, which include monocytes, macrophages, dendritic cells, and granulocytes, sit at the frontline of immune defense and tissue homeostasis, yet they are also among the immune compartments most visibly remodeled by ageing. These changes are influenced by several hallmarks of ageing and a central aim will be to disentangle intrinsic (cell-autonomous) from extrinsic (environment-driven) hallmarks of ageing and determine how they reshapes myeloid biology. Intrinsically, accumulated DNA damage, epigenetic drift, telomere attrition, mitochondrial dysfunction, impaired proteostasis/autophagy, and heightened cellular senescence programs can bias myeloid differentiation and survival, rewire metabolic set-points, and “pre-tune” signaling thresholds, leading to exaggerated inflammatory outputs or blunted immunological functions. Extrinsically, the ageing tissue environment shows chronic low-grade inflammation, altered cytokine and growth-factor availability, changes in stromal and endothelial cues, shifts in the microbiome and barrier integrity, and increased exposure to senescence-associated secretory phenotypes (SASP) can continuously imprint new activation states on myeloid cells, driving maladaptive inflammation, defective tissue-repair polarization, and compromised antigen presentation.
Together, these intrinsic and extrinsic changes coincide with age-associated shifts in hematopoiesis and a rising inflammatory baseline (“inflammageing”), yielding myeloid populations with altered pattern-recognition signaling, cytokine production, metabolic profiling and migratory behavior. These changes are highly relevant and linked to poorer vaccine responses, increased infection risk, chronic inflammatory pathology, and impaired tissue repair, yet the field still lacks a precise, cell-type-resolved definition of “myeloid ageing”.
PhD project: Defining Myeloid cell Ageing and its immunological impact on a single cell level
In our lab we have developed a number of tools to study myeloid cells on a single cell level. This includes single-cell RNAseq and large high-dimensional flow cytometry panels and a collection of transgenic mouse models specifically engineered for the reporting, lineage tracing, or conditional deletion of defined dendritic cell subsets. In this project the aim is to profile the tissue-specific myeloid cell single-cell landscape of young and old mice, establish tissue-specific murine models of premature ageing, define myeloid population specific SASP and mitochondrial signatures and thus unravel cell-intrinsic and extrinsic hallmarks of myeloid cell ageing.
This PhD requires a strong background in immunology, previous experience with the complex phenotyping of immune cells on a single-cell level and proficiency in working with in vivo animal models, including handling, experimental design and tissue processing and analysis. Experience in bioinformatics is a plus.
If you are interested in this project, please select Mayer (Ageing) as your project 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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