Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response |
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Authors: | 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 Shi Du Martin Eike Schleicher Erwin Stern David M Hämmerling G G ünterJ Nawroth Peter P Arnold Bernd |
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Affiliation: | Department of Molecular Immunology, Division of Tumor Immunology, German Cancer Research Center, Heidelberg, Germany. |
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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. |
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