Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response

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Issue Date
2004-06-01Author
Liliensiek, Birgit
Weigand, Markus A.
Bierhaus, Angelika
Nicklas, Werner
Kasper, Michael
Hofer, Stefan
Plachky, Jens
Gröne, Herman-Josef
Kurschus, Florian C.
Schmidt, Ann Marie
Yan, Shirley ShiDu
Martin, Eike
Schleicher, Erwin
Stern, David M.
Hämmerling, Günter J.
Nawroth, Peter P.
Arnold, Bernd
Publisher
American Society for Clinical Investigation
Type
Article
Article Version
Scholarly/refereed, publisher version
Metadata
Show full item recordAbstract
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.
Description
This is the publisher's version, also available electronically from http://www.jci.org/articles/view/18704
ISSN
0021-9738Collections
- Pharmacy Scholarly Works [293]
Citation
Liliensiek, Birgit et al. (2004). Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response. Journal of Clinical Investigation 113(11):1641-50. http://www.dx.doi.org/10.1172/JCI18704
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