File:PMC3109522 fmicb-01-00133-g001.png

English: F1: Diagram depicting survival mechanisms employed by L. pneumophila in human phagocytes. Upon entry into a human phagocyte, L. pneumophila becomes contained into a vacuole called Legionella-containing phagosome that avoids the typical fusion with the lysosome, and instead remodels into an ER-like vesicle allowing bacterial replication (1). L. pneumophila promotes the cleavage of Rabaptin-5 by caspase-3, thus preventing the default phagosome–lysosome fusion (2). L. pneumophila does not activate caspase-1 and -7 in human monocytes, consequently aborting the phagosome–lysosome fusion (3). This pathogen inhibits host cell apoptosis by up regulating anti-apoptotic genes (4). L. pneumophila controls the local balance of activating cytokines (INF-γ, TNF-α) that inhibit its replication, and inhibiting cytokines (IL-10) that allow its survival (5). L. pneumophila activates the NF-κB pathway to maintain host cell survival (6). L. pneumophila modulates other innate immune responses to establish a replicative niche (7).