Tuesday, October 06, 2009

Autophagy in Immunity Against Toxoplasma gondii

Curr Top Microbiol Immunol. 2009;335:251-65

Autophagy in Immunity Against Toxoplasma gondii

Subauste CS.

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

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 [PubMed - in process]

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