Host cell autophagy in immune response to zoonotic infections.

ΤίτλοςHost cell autophagy in immune response to zoonotic infections.
Publication TypeJournal Article
Year of Publication2012
AuthorsSkendros P, Mitroulis I
JournalClinical & developmental immunology
Volume2012
Pagination910525
Date Published2012
ISSN1740-2530
Λέξεις κλειδιάAnimals, Autophagy, Host-Pathogen Interactions, Humans, Signal Transduction, Zoonoses
Abstract

Autophagy is a fundamental homeostatic process in which cytoplasmic targets are sequestered within double-membraned autophagosomes and subsequently delivered to lysosomes for degradation. Accumulating evidence supports the pivotal role of autophagy in host defense against intracellular pathogens implicating both innate and adaptive immunity. Many of these pathogens cause common zoonotic infections worldwide. The induction of the autophagic machinery by innate immune receptors signaling, such as TLRs, NOD1/2, and p62/SQSTM1 in antigen-presenting cells results in inhibition of survival and elimination of invading pathogens. Furthermore, Th1 cytokines induce the autophagic process, whereas autophagy also contributes to antigen processing and MHC class II presentation, linking innate to adaptive immunity. However, several pathogens have developed strategies to avoid autophagy or exploit autophagic machinery to their advantage. This paper focuses on the role of host cell autophagy in the regulation of immune response against intracellular pathogens, emphasizing on selected bacterial and protozoan zoonoses.

DOI10.1155/2012/910525
Alternate JournalClin. Dev. Immunol.