TLR4 and infection: While studying the functional interplay between NE and ISP-2 during macrophage infection by Leishmania, Faria et al. [31, 32] demonstrated that two prominent phenotypes of Δisp2/3 mutants (upregulated phagocytosis and induction of ROS via the elastase/TLR4/PKR pathway) were completely reversed in cultures supplemented with three different inhibitors of serine peptidases: aprotinin [27], a non-specific inhibitor of Arg-hydrolyzers, MeOSuc-AAPV-CMK (NE inhibitor), and the L. major ISP-2 (soluble/recombinant).