Tissue homeostasis is maintained via a fine balance between pro- and anti-inflammatory signals, a balance that is lost when mitochondrial metabolism is compromised in T cells, resulting in impaired immunity, multimorbidity and inflammation.
The dynamic metabolism of T cells during an infection and upon nutrient stress depends indeed on the ability of T cells to fine tune their mitochondrial lipid composition (and in particular their content of the specific mitochondrial lipid cardiolipin).
Nevertheless, how different tissue specific microenvironments and immune cells crosstalk and determine the damage to different tissues as well as the systemic outcome of a metabolic dysfunction in T cell is poorly understood.
Our lab combines in vivo mouse phenotyping, classic immunology and biochemistry with quantitative proteomics and metabolomics to study the immune response in mouse models and patients affected by mitochondrial diseases.
29/04/2022 Dott. Mauro Corrado, CECAD center, University of Cologne (Germany)