We performed extensive multi-dimensional profiling of changes on the host side during viral-infection and uncovered a novel role for how the antiviral cytokine type I interferon orchestrates the metabolic reprogramming of the liver (DOI: 10.1016/j.immuni.2019.10.014). More specifically, we could delineate how the central metabolic pathway of the urea cycle is perturbed during infection and how this feed backs onto antiviral T cell responses. This work has brought new attention to hepatocytes as key regulatory cells of the immune response. Moreover, we dissected additional metabolic pathways in the liver such as the tryptophane-kynurenine pathway and established paradigms for how infections induce changes in systemic immunometabolism (DOI: 10.1371/journal.ppat.1008973). We In also described a novel role for the lipid-sensing receptor TREM2 and how it modulates hepatitis during viral infection (DOI: 10.1038/s41598-017-10637-y).
Further to investigating infection-associated changes in the liver, we became interested into systemic immunometabolic changes and took a particular focus on adipose and muscle tissue. In diseases such as cancer, chronic inflammation and infection, wide-spread metabolic and inflammatory alterations are found and associated with the devastating disease cachexia. This is manifested as body weight loss, reduction of fat and lean body mass, lack of appetite, lethargy amongst other symptoms, which cannot be reversed by nutritional interventions. Currently, there’s an incomplete understanding of the underlying mechanisms and standard therapies are lacking. We uncovered a previously unrecognized role by our T cell responses mediate cachexia during viral infection and established a novel model to study infection-associated cachexia (Baazim et al. 2019, DOI: 10.1038/s41590-019-0397-y). We discussed its implication and broader context of how the field of immunology can both deliver and benefit from studying this important disease of cachexia in a review (Baazim et al. 2021, DOI: 10.1038/s41577-021-00624-w).
