TY - JOUR
T1 - Autophagy in the regulation of pathogen replication and adaptive immunity
AU - Randow, Felix
AU - Münz, Christian
N1 - Funding Information:
Research in the laboratory of C.M. is supported by grants from the National Cancer Institute (R01CA108609), the Sassella Foundation (10/02), Cancer Research Switzerland (KFS-02652-08-2010), the Association for International Cancer Research (11-0516), the Vontobel Foundation, the Baugarten Foundation, Novartis and the Swiss National Science Foundation (310030_126995). Work in the laboratory of F.R. is supported by the Medical Research Council (U105170648) and The National Association for Colitis and Crohn's Disease (M/11/3).
PY - 2012/10
Y1 - 2012/10
N2 - Autophagy is an evolutionarily conserved homeostatic process by which cells deliver cytoplasmic material for degradation into lysosomes. Autophagy may have evolved as a nutrient-providing homeostatic pathway induced upon starvation, but with the acquisition of cargo receptors, autophagy has become an important cellular defence mechanism as well as a generator of antigenic peptides for major histocompatibility complex (MHC) presentation. We propose that autophagy efficiently protects against microbes encountering the cytosolic environment accidentally, for example, upon phagosomal damage, whereas pathogens routinely accessing the host cytosol have evolved to avoid or even benefit from autophagy.
AB - Autophagy is an evolutionarily conserved homeostatic process by which cells deliver cytoplasmic material for degradation into lysosomes. Autophagy may have evolved as a nutrient-providing homeostatic pathway induced upon starvation, but with the acquisition of cargo receptors, autophagy has become an important cellular defence mechanism as well as a generator of antigenic peptides for major histocompatibility complex (MHC) presentation. We propose that autophagy efficiently protects against microbes encountering the cytosolic environment accidentally, for example, upon phagosomal damage, whereas pathogens routinely accessing the host cytosol have evolved to avoid or even benefit from autophagy.
UR - https://www.scopus.com/pages/publications/84866767594
U2 - 10.1016/j.it.2012.06.003
DO - 10.1016/j.it.2012.06.003
M3 - Review article
C2 - 22796170
AN - SCOPUS:84866767594
SN - 1471-4906
VL - 33
SP - 475
EP - 487
JO - Trends in Immunology
JF - Trends in Immunology
IS - 10
ER -