%0 Journal Article
%T Autophagy in herpesvirus immune control and immune escape
%A Graham S Taylor
%A Josef Mautner
%A Christian M¨šnz
%J Herpesviridae
%D 2011
%I BioMed Central
%R 10.1186/2042-4280-2-2
%X Mammalian cells use primarily two proteolytic systems to catabolise intra- and extracellular material for energy and macromolecular building block generation. These are proteasomes and lysosomes. While proteasomes degrade soluble ubiquitinated proteins, lysosomes destroy ubiquitinated protein aggregates and cell organelles. Interestingly, these degradation mechanisms can also be used to eliminate pathogens and process their fragments for presentation to the immune system [1]. Access of substrates to these proteolytic, and in the case of lysosomes generally hydrolytic, machineries is tightly regulated by the 19 s cap complex for the proteasome, and endocytosis, vesicular sorting and autophagy for lysosomes.In this context, autophagy delivers cytoplasmic constituents into lysosomes. Three autophagic pathways have been identified [2]. The first pathway, microautophagy, is a process in which substrates bud into the lysosomal lumen for degradation, but has thus far not been described in higher eukaryotes. The second pathway, chaperone mediated autophagy (CMA), transports proteins that contain a KFERQ like recognition sequence across the lysosomal membrane sequence into the lysosomal lumen. This transport is assisted by cytosolic and lysosomal chaperones as well as LAMP2a. The third pathway, macroautophagy, is currently the best characterised of the three. Macroautophagy employs 34 gene products, so called autophagy related (Atg) proteins, to construct a vesicle, the autophagosome, around its substrate and deliver it for fusion with lysosomes [3]. Autophagosomes are assembled from membranes of the rough endoplasmic reticulum, Golgi apparatus, outer nuclear or mitochondrial membrane, and the cell membrane [4-11]. Autophagosome assembly nucleates around type III phosphatidylinositol (PI) 3 kinase complexes, containing the PI3 kinase hVps34, hVps15, Atg14L and Atg6/Beclin-1 (Figure 1). Elongation of the autophagosome membrane to an isolation membrane is then achieved with th
%U http://www.herpesviridae.org/content/2/1/2