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