Abstract

The innate immune system has been considered as an ancient system and less important than the adaptive immune system. However, the interest in innate immunity has grown significantly in the past few years marked by the identification of Toll-like receptors, a member of pattern recognition receptors (PRRs). The PRRs are crucial for the identification of self- and non-self-antigen and play a role in the initiation of signaling events that activate the effective immune response. These sensor signals through interweaving signaling cascades which result in the production of interferons and cytokines as the effector of immune system. Ubiquitin and ubiquitin-like modifiers (UBLs) actively mediate the rapid and versatile regulatory processes that initiate the activation of the innate immune system cascade. The seven in absentia homolog (SIAH) is a potent RING finger E3 ubiquitin ligase that is known to involve in several stress responses, including hypoxia, oxidative stress, DNA damage stress, and inflammation. In this review, the role of SIAH will be discussed as an E3 ubiquitin ligase on the regulation of innate immune.

Highlights

  • The innate immunity provides a first line of host defense against invading pathogens

  • Ubiquitin and ubiquitin-like modifiers (UBLs) actively mediate the rapid and versatile regulatory processes that initiate the activation of the innate immune system cascade

  • The seven in absentia homolog (SIAH) is a potent RING finger E3 ubiquitin ligase that is known to involve in several stress responses, including hypoxia, oxidative stress, DNA damage stress, and inflammation

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Summary

Introduction

The innate immunity provides a first line of host defense against invading pathogens. The role of SIAH will be discussed as an E3 ubiquitin ligase on the regulation of innate immune. The pathogens binding with PRRs activate innate immune response through various signaling cascades and activate the pro-inflammatory transcription factors such as activator protein 1 (AP-1), nuclear factor-kappa B (NF-κB), and/or one or more members of the interferon (IFN) regulatory factor family which, in turn, lead to the release of cytokines and IFNs [1,2].

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