Immune Frontlines: Rapid Defenders and the Metabolic War Within

Host: René van Lier
Date and Time: Tuesday december 16, 1600-1730. Drinks afterwards
Place: Q-auditorium

Klaas van Gisbergen

Physiology and Cancer Programme, Champalimaud Research, Champalimaud Foundation, 1400-038 Lisbon, Portugal

The quick and the dead: a tale of resident memory T cells in infection and cancer

To establish fast and powerful immune responses against frequently encountered viruses, T cells differentiate into distinct subsets of circulating and resident memory T cells. Our lab is interested in how T cells make choices to diversify in different lineages in response to infection. Previously, we discovered and characterized a transcription factor that we named Hobit for Homologue of Blimp-1 in T cells (van Gisbergen, Nature Immunology, 2012), and we established how resident memory T cells separate from circulating memory T cells under the control of Hobit and Blimp-1 (Mackay, Science, 2016). Next, we have exploited Hobit as a tool to study how resident memory T cells develop in primary responses (Parga Vidal, Science Immunology, 2021), how these cells contribute to secondary immune responses against re-encountered pathogens (Behr, Nature Immunology, 2020), and how they are constrained to prevent tissue damage (Stark, Science Immunology, 2018).  In the summer of 2023, my lab has moved from Sanquin Research in Amsterdam to Champalimaud Research in Lisbon, where we have continued to work on how T cells differentiate in response to infection and tumor challenge.

Felix Wensveen

Department for Histology and Embryology, University of Rijeka, Faculty of Medicine, Rijeka, Croatia

War-time metabolism: How the immune system rewires the body to fight infection

When we get sick we feel miserable. This so called ‘sickness metabolism’ is not caused by the pathogen, but is a highly conserved mechanism controlled by the activated immune system. How this happens and how it benefits the immune response is the focus of the group of Felix Wensveen. His team investigates which infection-induced, tissue-derived signals activate immune cells and mediate their modulation of organ function and thereby systemic metabolism (Wensveen Nat Immunol. 2015, Krapić Science Immunol. 2025). A specific focus is on the Th1 cytokine IFNγ and how it modulates systemic availability of metabolites such as glucose and free fatty acids (Šestan Nat Immunol. 2024). In addition, their team questions how systemic alteration of metabolites and hormones affect the immune response, with a particular interest in T cells (Kavazović Diabetes 2022). Importantly, the team of Prof. Wensveen studies how these antiviral defense mechanism derail in context of obesity and contribute to the development of metabolic disease (Šestan Immunity 2018, Gašparini Diab Res Clin Pract. 2024).