Receptor for Advanced Glycation End Products (RAGE) Regulates Sepsis but Not the Adaptive Immune Response

Overview

Journal J Clin Invest

Specialty General Medicine

Date 2004 Jun 3

PMID 15173891

Citations 242

Authors

Birgit Liliensiek

Markus A Weigand

Angelika Bierhaus

Werner Nicklas

Michael Kasper

Stefan Hofer

Jens Plachky

Herman-Josef Grone

Florian C Kurschus

Ann Marie Schmidt

Shi Du Yan

Eike Martin

Erwin Schleicher

David M Stern

G unterJ Hammerling G

Peter P Nawroth

Bernd Arnold

Affiliations

Soon will be listed here.

Abstract

While the initiation of the adaptive and innate immune response is well understood, less is known about cellular mechanisms propagating inflammation. The receptor for advanced glycation end products (RAGE), a transmembrane receptor of the immunoglobulin superfamily, leads to perpetuated cell activation. Using novel animal models with defective or tissue-specific RAGE expression, we show that in these animal models RAGE does not play a role in the adaptive immune response. However, deletion of RAGE provides protection from the lethal effects of septic shock caused by cecal ligation and puncture. Such protection is reversed by reconstitution of RAGE in endothelial and hematopoietic cells. These results indicate that the innate immune response is controlled by pattern-recognition receptors not only at the initiating steps but also at the phase of perpetuation.

Citing Articles

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