Staff Scientist NIAID, NIH Corvallis, Montana, United States
Pulmonary infections often fail to generate durable immune memory, but the underlying mechanism(s) remain unclear. In a model of bacterial infection, poor protection after challenge correlated with rapid IFN-γ production by lung resident T cells, IDO1 upregulation within endothelial cells, tryptophan depletion, and impaired T cell proliferation. Spatial imaging showed T cells clustered near IDO1+ CD31+ endothelium, but not at infection foci, suggesting that T cell–endothelial crosstalk undermines the development of effective immune memory.
