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PhD Position: Immunology: Defining Hallmarks of Myeloid cell ageing single cell level; m​/f​/d

Job in Germany, Pike County, Ohio, USA
Listing for: International PhD Programme (IPP) Mainz
Full Time, Seasonal/Temporary position
Listed on 2026-03-03
Job specializations:
  • Research/Development
    Research Scientist, Immunology Research
  • Healthcare
Salary/Wage Range or Industry Benchmark: 80000 - 100000 USD Yearly USD 80000.00 100000.00 YEAR
Job Description & How to Apply Below
Position: PhD Position: Immunology: Defining Hallmarks of Myeloid cell ageing on a single cell level (m/f/d)
Location: Germany

Organisation/Company International PhD Programme (IPP) Mainz Department Institute of Molecular Biology Research Field Biological sciences » Biology Researcher Profile First Stage Researcher (R1) Positions PhD Positions Final date to receive applications 1 Apr 2026 - 12:00 (Europe/Berlin) Country Germany Type of Contract Temporary Job Status Full-time Offer Starting Date 1 Jul 2026 Is the job funded through the EU Research Framework Programme?

Not funded by a EU programme Is the Job related to staff position within a Research Infrastructure? No

Offer Description

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.

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…

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