Affiliation:
1. Department of Microbiology & Molecular Biology, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111, USA
2. Howard Hughes Medical Institute & Molecular Biology, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111, USA
Abstract
ABSTRACT: Macrophages are the front line of immune defense against invading microbes. Microbes, however, have evolved numerous and diverse mechanisms to thwart these host immune defenses and thrive intracellularly. Legionella pneumophila, a Gram-negative pathogen of amoebal and mammalian phagocytes, is one such microbe. In humans, it causes a potentially fatal pneumonia referred to as Legionnaires’ disease. Armed with the Icm/Dot type IV secretion system, which is required for virulence, and approximately 300 translocated proteins, Legionella is able to enter host cells, direct the biogenesis of its own vacuolar compartment, and establish a replicative niche, where it grows to high levels before lysing the host cell. Efforts to understand the pathogenesis of this bacterium have focused on characterizing the molecular activities of its many effectors. In this article, we highlight recent strides that have been made in understanding how Legionella effectors mediate host–pathogen interactions.
Subject
Microbiology (medical),Microbiology
Cited by
81 articles.
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