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.
The research group of Johannes Mayer offers a PhD project that investigates myeloid cells, which include monocytes, macrophages, dendritic cells, and granulocytes. These cells sit at the frontline of immune defense and tissue homeostasis, yet they are also among the immune compartments most visibly remodeled by ageing. The project aims to disentangle intrinsic (cell‑autonomous) from extrinsic (environment‑driven) hallmarks of ageing and determine how they reshapes myeloid biology.
Intrinsic changes such as accumulated DNA damage, epigenetic drift, telomere attrition, mitochondrial dysfunction, impaired proteostasis and heightened cellular senescence bias myeloid differentiation and survival, rewire metabolic set‑points, and “pre‑tune” signaling thresholds. Extrinsic changes include 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). These factors 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”.
In our lab we have developed a number of tools to study myeloid cells on a single‑cell level, including single‑cell RNAseq, high‑dimensional flow cytometry panels, and transgenic mouse models for reporter, lineage‑tracing and conditional deletion of defined dendritic cell subsets. The goal of the project is to profile the tissue‑specific myeloid cell landscape of young and old mice, establish tissue‑specific murine models of premature ageing, define myeloid population‑specific SASP and mitochondrial signatures, and thereby unravel cell‑intrinsic and extrinsic hallmarks of myeloid cell ageing.
This PhD requires a strong background in immunology and experience with the complex phenotyping of immune cells on a single‑cell level, as well as proficiency in working with in vivo animal models, including handling, experimental design and tissue processing and analysis. Experience in bioinformatics is a plus.
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.
#J-18808-LjbffrVeröffentlichungsdatum:
02 Mär 2026Standort:
MainzTyp:
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2+ yearsArbeitsverhältnis:
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