These studies led to the discovery of type III secretion (T3S), a concept that was pioneered in parallel by H. Wolf-Watz in Umea, Sweden, and presented in (Cornelis and Wolf-Watz, Mol. Microbiol., 1997, 23: 861-67). T3S is a mechanism by which many Gram- bacteria inject "effector" proteins into the cytosol of animal, plant or insect cells. The effectors disarm the target cell by sabotaging the cellular signaling network. The T3S apparatus, called injectisome, is a complex nanosyringe made of more than 25 different proteins. It consists of a transmembrane basal body and a ca 60-nm long needle protruding from the surface. Yersinia utilize such a system to inject anti-phagocytic and anti-inflammatory effector proteins (called Yops) into cells of the host immune system. The milestones of this research in Guy's laboratory are a) the initial observation that Yops are secreted without the removal of a classical signal sequence (Michiels et al., Infect. Immun. 1990, 58: 2840-9; Michiels and Cornelis, J. Bacteriol. 1991, 173: 1677-85) by T3S System (Michiels et al., J. Bacteriol. 1991, 173: 4994-5009); b) the discovery of a new class of chaperones which assist secretion of some Yop proteins (Wattiau and Cornelis, Mol. Microbiol. 1993, 8: 123-31; Wattiau et al., PNAS 1994, 91: 10493-7; Letzelter et al., EMBO J. 2007, 26: 3015-24); c) the introduction of a reporter system based on the calmodulin-dependant adenylate-cyclase to demonstrate that effectors are injected by the bacterium into the cytosol of target cells (Sory and Cornelis, Mol. Microbiol. 1994, 14: 583-94; Sory et al., PNAS, 1995, 92: 11998-12002; Boland et al., EMBO J. 1996, 15: 5191-5201); d) the demonstration that effector YopP prevents the release of TNF-alpha by macrophages and causes their apoptosis (Mills et al., PNAS 1997, 94: 12638-43; Boland and Cornelis, Infect. Immun. 1998, 66: 1878-84).