Autophagy in immunity against Toxoplasma gondii.
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.
Department of Ophthalmology and Visual Sciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. carlos.subauste@case.edu
Carlos S
CS
Subauste
D000818:Animals; D001343:Autophagy / Q000276:immunology*; D019013:CD40 Antigens / Q000276:immunology; D006801:Humans; D008247:Lysosomes / Q000276:immunology / Q000469:parasitology; D014122:Toxoplasma / Q000276:immunology*; D014123:Toxoplasmosis / Q000276:immunology*; D014617:Vacuoles / Q000276:immunology / Q000469:parasitology
D019013:CD40 Antigens