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
. 2013:2013:124614.
doi: 10.1155/2013/124614. Epub 2013 Jun 23.

TLR2 and TLR4 in the brain injury caused by cerebral ischemia and reperfusion

Ying Wang  1 , Pengfei Ge, Yuhong Zhu
Affiliations
Review

TLR2 and TLR4 in the brain injury caused by cerebral ischemia and reperfusion

Ying Wang et al. Mediators Inflamm. 2013.

Abstract

Brain injury caused by cerebral ischemia/reperfusion is a complicated pathophysiological course, in which inflammation is thought to play an important role. Toll-like receptors are a type of transmembrane proteins, which can recognize either exogenous pathogen-associated molecular patterns or endogenous stress or damage-associated molecular patterns in the innate immune system and initiate inflammatory responses. Among Toll-like receptors, TLR2 and TLR4 are found to be more important than others in the pathological progression of cerebral injury due to ischemia and reperfusion. This review will focus on the biological characteristics and functions of TLR2 and TLR4 and their downstream signal pathways.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Brain injury caused by cerebral ischemia/reperfusion is a complicated pathophysiological course, in which TLR2 and TLR4 are thought to play an important role. TLR2 and TLR4 play crucial roles in modulating inflammatory response caused by cerebral ischemia and reperfusion via linking to their endogenous ligands and then recruit specific adaptors within cells. TLRs signal activates the transcription factors and generates cytokines and chemokines via intracellular pathways.
See this image and copyright information in PMC

References

    1. Nusslein-Volhard C, Wieschaus E. Mutations affecting segment number and polarity in Drosophila . Nature. 1980;287(5785):795–801. - PubMed
    1. Steward R, McNally FJ, Schedl P. Isolation of the dorsal locus of Drosophila . Nature. 1984;311(5983):262–265. - PubMed
    1. Medzhitov R, Preston-Hurlburt P, Janeway CA., Jr. A human homologue of the Drosophila toll protein signals activation of adaptive immunity. Nature. 1997;388(6640):394–397. - PubMed
    1. Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity. Cell. 2006;124(4):783–801. - PubMed
    1. Gordon S. Pattern recognition receptors: doubling up for the innate immune response. Cell. 2002;111(7):927–930. - PubMed

Publication types

LinkOut - more resources