Macrophages are major effector cells of the innate immune system, and appropriate
regulation of macrophage function requires the integration of multiple signalling inputs
derived from the recognition of host factors (eg interferon-γ/IFNγ) and pathogen products (eg
toll-like receptor/TLR agonists). The profound effects of IFNγ pre-treatment (“priming”) on
TLR-induced macrophage activation have long been recognised, but many of the
mechanisms underlying the priming phenotype have only recently been identified. This …