Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Nov:205:115246.
doi: 10.1016/j.bcp.2022.115246. Epub 2022 Sep 8.

Bifurcation of signalling in human innate immune pathways to NF-kB and IRF family activation

Affiliations
Free article
Review

Bifurcation of signalling in human innate immune pathways to NF-kB and IRF family activation

Aleksandra Kusiak et al. Biochem Pharmacol. 2022 Nov.
Free article

Abstract

The human innate immune response can be activated through a wide range of stimuli. This multi-faceted system can be triggered by a range of immunostimulants including pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). These stimuli drive intracellular signalling pathways that branch off downstream to activate several distinct transcription factors. The two most impactful of which in innate immune outcomes are the NF-κB and the IRF family members. Both transcription factor families play defining roles in driving inflammation as well as the antiviral response. Pathways leading to their simultaneous activation share common upstream components but eventually distinct regulators which directly facilitate their activation. This review will discuss the current state of knowledge about what is known about how these pathways bifurcate to activate NF-κB and IRF family members.

Keywords: IRF; Innate immunity; NF-kB; Pro-inflammatory; Signal transduction; Signalling.

PubMed Disclaimer

Conflict of interest statement

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Publication types

MeSH terms

Substances

LinkOut - more resources