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We are looking for postdoctoral applicants in the field of cardiovascular immunology 



The aim of the postdoctoral project is to study the innate and adaptive immune cell crosstalk in cardiac injury responses, in particular within pericardial fat-associated lymphoid clusters. The postdoc shall perform a detailed imaging of pericardial lymphoid clusters in response to cardiac injury, comparative immunophenotyping of circulating, cardiac and pericardial immune cells as well as immune cell tracking.


The project involves the following techniques:

-Experimental mouse models of myocardial infarction and pressure overload-induced cardiac remodeling

-Flow cytometry, advanced imaging methods (e.g. two-photon laser scanning microscopy)

-Single cell RNA sequencing

-Functional in vitro assays


Your profile:

Eligible candidates should have experience with (cardiovascular) mouse models, immunological and bioimaging techniques. Experience with transcriptomic data analysis would be an additional advantage. They should have a strong motivation and team spirit as well as the curiosity, enthusiasm and driving force to bring a scientific question to the utmost end. German language skills are a plus, but not essential. However, solid English skills written and spoken are mandatory. We offer a stimulating international research environment, excellent equipment and close interaction to benefit from the broad expertise of the various groups in our institute ( The project is funded by the German Centre for Cardiovascular Research (DZHK) and associated to the SFB (Collaborative Research Center 1123) “Atherosclerosis - Mechanisms and Networks of Novel Therapeutic Targets”. For more information, please visit the websites and


Relevant publications:

  • Horckmans et al. and Steffens S (2017). Neutrophils orchestrate post-myocardial infarction healing by polarizing macrophages towards a reparative phenotype. European Heart Journal, 38(3):187-197
  • Horckmans et al. and Steffens S (2018). Pericardial adipose tissue regulates granulopoiesis, fibrosis and cardiac function after myocardial infarction. Circulation 137(9):948-960
  • Schloss et al. and Steffens S (2018). 2-arachidonoylglycerol mobilizes myeloid cells and worsens heart function after acute myocardial infarction. Cardiovasc Res. 2018 Sep 28.


Interested candidates should submit their application (including CV, publication list and references) via email to Prof. Dr. rer. nat. Sabine Steffens:


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Prof. Dr. med. Christian Weber