This leads to the transcription and expression of hundreds of genes, particularly pro-inflammatory cytokines, including Interleukin-1 −6 −18 (IL-1 IL-6 IL-18), Tumor Necrosis Factor α (TNF-α), and type I Interferon (type I IFN) ( 3). Upon stimulation of PRRs, several transcription factors are activated and translocate to the nucleus. Pattern Recognition Receptors (PRRs) orchestrate the detection of Pathogen-Associated Molecular Patterns (PAMPs), triggering an anti-microbial response by an important shift in transcriptional activity ( 2). Upon viral infection, host cells possess an arsenal of innate responses to protect themselves and their neighbors, counteracting pathogen replication and spread. Among their cellular functions both systems are highly involved in the regulation of innate immune responses upon pathogenic infection. However, some specificities exist between both mechanisms the Ubiquitin-Proteasome System is mainly responsible for the degradation of short-lived proteins, while autophagy is able to degrade several kinds of substrates, such as long-lived proteins, aggregates, or entire organelles.
In this review we describe several links between autophagy and regulation of innate immune responses and we provide an overview of how viruses exploit these links for their own benefit.Ĭellular catabolism is ensured by both the Ubiquitin Proteasome System and the process of autophagy acting in a coordinated manner in order to maintain homeostasis ( 1). Published reports related to this last viral strategy have extensively grown in recent years. Controlling the signals that lead to production of these cytokines is a perfect way for viruses to escape from innate immune responses and establish successful infection.
The control of viral replication and spread involves the production of anti-viral cytokines. The arms race between hosts and pathogens has led some viruses to evolve strategies that enable them to benefit from autophagy, either by directly hijacking the autophagy pathway for their life cycle, or by using its regulatory functions in innate immunity. Many studies have shown that it can also play a role in the control of innate immunity by preventing exacerbated inflammation and its harmful effects toward the host.
Autophagy dysfunction is often associated with inflammatory diseases. This process is a key player in innate immunity and its activation has anti-microbial effects by directly targeting pathogens and also by regulating innate immune responses.
Autophagy is a lysosomal degradation pathway for intracellular components and is highly conserved across eukaryotes.
0 kommentar(er)
