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Curr Top Microbiol Immunol. 2009;335:251-65. doi: 10.1007/978-3-642-00302-8_12.

Autophagy in immunity against Toxoplasma gondii.

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1
Department of Ophthalmology and Visual Sciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. carlos.subauste@case.edu

Abstract

A decisive outcome during host-pathogen interaction is governed by whether pathogen-containing vacuoles fuse with lysosomes. Fusion with lysosomes typically kills microbes. Toxoplasma gondii represents a classical example of an intracellular pathogen that survives within host cells by preventing the endosomal-lysosomal compartments from fusing with the vacuoles that contain the pathogen. Thus, T. gondii provides an excellent model to determine if the immune system can target a pathogen for lysosomal degradation. CD40, a major regulator of cell-mediated immunity, activates macrophages to kill T. gondii through a process that requires recruitment of autophagosomes around the parasitophorous vacuole, leading to lysosomal degradation of the parasite. These studies demonstrate that cell-mediated immunity can activate autophagy to kill a pathogen. CD40-induced autophagy likely contributes to resistance against T. gondii, particularly in neural tissues, the main sites affected by this pathogen.

PMID:
19802569
DOI:
10.1007/978-3-642-00302-8_12
[Indexed for MEDLINE]
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