New metabolic signatures of human T-cells uncovered

Dr. Alex M Dickens (left), Dr. Partho Sen, Dr. Syed Bilal Ahmad Andrabi and Dr. Tanja Buchacher represent Systems Medicine group headed by Professor Matej Orešič and Molecular Systems Immunology group headed by Professor Riitta Lahesmaa.

InFLAMES-researchers at Turku Bioscience in joint collaboration with the Örebro University, Sweden have uncovered new ‘metabolic signatures’ of human CD4+ T-cells.

T-cells are white blood cells that coordinate our immune response and provide protection against pathogens and cancer. Abnormally functioning T-cells may lead to the development of cancer or autoimmune disorders.im

Scientists at University of Turku and Örebro University studied metabolism of human T-cells with sophisticated, cutting edge technologies such as computer-based modelling, high throughput lipidomics, transcriptomics techniques, and conducting in vitro knockdown experiments. They identified that certain molecular lipids such as ceramides and glycosphingolipids play an important role in the functioning of human T-cells.

– Our results provide basis for engineering and manipulating metabolism of human T-cells to treat immune-mediated diseases, authors say.

Manipulating human T-cell metabolism to modulate their early specification for therapeutic purposes is a new paradigm and offers significant new options in the future to develop safe and effective therapies for cancer and autoimmune diseases. Since ceramides are lipotoxic lipids that are commonly elevated in obesity and insulin resistance,  the study may also offer clues about the poorly understood overlap in co-morbidities between specific immune-mediated diseases characterized by expression of proinflammatory cytokines and metabolic diseases, such as has been found to occur in COVID-19.

Article was published in Cell Reports, titled as “Quantitative genome-scale metabolic modeling of human CD4+ T-cell differentiation reveals subset-specific regulation of glycosphingolipid pathways”. Link to the article.