NF-\u03baB signaling in inflammation

Ting Liu,Donghyun Joo,Lingyun Zhang,Shao-Cong Sun

doi:10.1038/sigtrans.2017.23

Abstract

The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition.

Highlights

Nuclear factor-κB (NF-κB) represents a family of inducible transcription factors, which regulates a large array of genes involved in different processes of the immune and inflammatory responses.[1]
Th2 responses and allergic airway inflammation, which appears to involve induction of the lineage transcription factor Gata3.42 Several NF-κB members have been shown to promote Th17 in vitro conditions, only trigger weak activation of noncanonical NF-κB, which can be greatly enhanced by cross-linking the TNF receptor (TNFR) OX40.51,53 Collectively, these findings suggest that both canonical responses
It is well accepted that NF-κB serves as a central inflammatory mediator that responds to a large variety of immune receptors

Summary

Introduction

Nuclear factor-κB (NF-κB) represents a family of inducible transcription factors, which regulates a large array of genes involved in different processes of the immune and inflammatory responses.[1].

Results

Conclusion