In adoptive transfer settings, the production of IFNγ by CD4+ T cells was sufficient to drive LT-HSC exhaustion defining this pro-inflammatory cytokine as a key regulator of hematopoiesis during infection with L. donovani. Strikingly, the absence of CD4+ T cell-intrinsic TNF signalling prevented their expansion in the BM of infected mice, and limited their potential to produce IFNγ, indicating that TNF plays a central upstream role in regulating the BM T cell compartment during infection. This evidence concerns the gene IFNG and infection.