Legionella pneumophila modulates macrophage functions through epigenetic reprogramming via C-type lectin receptors
Legionella pneumophila is a pathogen which can lead to a severe form of pneumonia in humans known as Legionnaires disease after replication in alveolar macrophages. Viable L. pneumophila actively secrete effector molecules to modulate the hosts immune response. Here, we report that L. pneumophila-derived factors reprogram macrophages into a tolerogenic state, a process to which C-type lectin receptors markedly contributes.