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Figure 1 | Critical Care

Figure 1

From: The role of receptor for advanced glycation endproducts (RAGE) in infection

Figure 1

Putative involvement of the receptor for advanced glycation endproducts (RAGE) during infection. The damage-associated molecular patterns (DAMPs), high-mobility group box 1 (HMGB1) and S100A12, are released during infection ([15, 17], and unpublished data) and bind to and activate RAGE. It has to be determined whether other S100 proteins and other DAMPs are RAGE ligands (indicated as purple shapes) released during infection. It would be interesting to investigate whether RAGE can directly bind to, become activated and mount a first immune reaction after ligation with specific PAMPs as well. Engagement of RAGE by its ligands results in receptor-dependent signaling and activation of NF-κB leading to a pro-inflammatory response; the signaling pathway is largely unknown. In addition, RAGE interacts as an endothelial (and epithelial) adhesion receptor with the leukocyte integrin, CD11b/CD18 (Mac-1) (lower section) [8]. Furthermore, lateral (in cis) RAGE-Mac-1 interaction on the leukocyte surface is mediated by HMGB1 and activates Mac-1-intercellular adhesion molecule (ICAM)-1 dependent adhesion and migration and augments leukocyte recruitment [27] (indicated by the blue line and blue "+"). Moreover, a recent report shows that endothelially expressed RAGE acts in concert with ICAM-1 in mediating β2 integrin-dependent leukocyte adhesion during acute trauma-induced inflammation [28] (indicated by the green line and green "+").

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