Sebastian Weis

This paper identifies transient GSK3β activation as a mechanism promoting disease tolerance to sepsis through hypometabolism, without affecting pathogen burden.

This study identifies CXCL5 as a factor that increases alveolar-epithelial barrier permeability in acute lung injury, independent of neutrophil recruitment.

This study identifies adipocyte lipolysis as a critical metabolic process that prevents sepsis in mice by supporting energy metabolism and thermoregulation through insulin signaling, without affecting bacterial burden.

This study shows that type 1 immunity, via IFNγ signaling, protects intestinal tissue from damage during helminth infection without reducing parasite burden.

This study shows that monocyte-derived macrophages regulate energy homeostasis by responding to iron metabolism dysregulation in parenchyma cells.

The paper shows that exosomes from aged mice can cross the blood-brain barrier and activate glial cells, as indicated by increased GFAP expression.

The paper shows that loss of GGTA1 function in mice increases resistance to sepsis via enhanced IgG-Fc gamma receptor binding but causes earlier reproductive senescence, suggesting a trade-off that may explain primate evolution.