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Epicardial adipose tissue (EAT) is a visceral fat that surrounds the myocardium and secretes inflammatory mediators. EAT has been associated with cardiovascular risk factors and cardiovascular disease manifestations. A high density of lymphoid clusters with elevated T cell numbers have been detected in EAT in repAMI. EAT has been suggested to be crucially involved in repAMI response mechanisms as a source of T cells and regulator of inflammation. However, the functional phenotype of these specific sets of immune cells has been incompletely characterized.

Molecular and functional characterization of different T cell subsets in EAT and other thoracic fat depots from human patients and repAMI mice to understand their impact on myocardial infarct response mechanisms. Specific questions are:

• Which T cell subsets are present/ prominent in EAT and other thoracic fat depots?
• What is the molecular and functional phenotype of EAT derived T cells?
• Which molecules are important for the molecular and functional phenotype of T cells in the context of repAMI?
• Where are the T cells localized within the EAT and other thoracic fat depots?
• Are there differences between human samples and adipose-tissue from repAMI mice?

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T cells invade the heart from epicardial layer​

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Analysis of T cells in EAT from healthy and repAMI mice
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Principal Investigators

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