The bone marrow undergoes profound age-related changes, including a state of persistent, low-grade inflammation known as inflammageing. Ageing also alters the immune system, a phenomenon termed immunosenescence. This leads to weaker responses to infections and vaccines, impaired tissue repair, and chronic systemic inflammation. T cells are particularly affected, and latent infections that are prevalent in the eldery, such as Cytomegalovirus or Epstein–Barr virus, can further reshape both innate and adaptive immunity. These changes are linked to accelerated immune ageing and increased cardiovascular risk. Taking advantage of a recently established experimental model of common viral infections we will determine how immunosenescence within the bone marrow affects megakaryocyte and platelet function. We will investigate how (i) the age-related accumulation of IFN-γ–producing T cells and (ii) pathogen-induced immune senescence alter megakaryocyte and platelet biology, and their interactions with other cell types.

Our approaches include spectral flow cytometry, multiplex and dynamic imaging, single-cell and spatial transcriptomics, experimental mouse and infection models, and functional assays of immune cells and platelets.

By integrating immunology, infection biology, and platelet research, this project seeks to reveal how an ageing immune system reshapes platelet formation and function. Ultimately, the findings may help explain age-related changes in platelet function and cardiovascular risk, and open new avenues to promote healthy ageing.