|
Source | Disease model | Properties of C5aR2 | Refs |
|
B. Lu, Harvard Medical School, USA | IC-induced acute lung injury | Anti-inflammation | [34] |
Anti-mMPO-induced ANCA NCGN | Anti-inflammation | [88] |
CLP-induced sepsis and in vitro assays on leukocytes | Proinflammation and indispensable for HMGB-1 release | [7] |
CLP-induced sepsis | On CMs—proinflammation and causes cardiac dysfunction | [75, 76, 78] |
Acute pyelonephritis | Proinflammation | [72] |
Renal I/R injury | Proinflammation | [73] |
Experimental cerebral malaria | No function※ | [124] |
S. aureus bloodstream infection | Anti-inflammation | [125] |
AKI induced by LPS, IC, or C5a | Proinflammation | [71] |
Genotyping and breeding in University of Michigan according to the method of Dr. Craig Gerard | CLP-induced sepsis | Indispensable for G-CSF release by macrophages | [79] |
CLP-induced sepsis | On CMs—proinflammation: activation of the cardiac NLRP3 inflammasome | [77] |
Professor A. Klos, Hannover Medical School, Germany | Wire-induced endothelial denudation of the carotid artery, diet-induced atherosclerosis | Proinflammation | [66] |
The Jackson Laboratory | In vitro atherosclerosis model | On PBMCs and BMDMs—proinflammation | [87] |
Lexicon Genetics, the Woodlands, Texas | Thioglycollate-induced peritonitis and air-pouch inflammation | Proinflammation | [68] |
| LPS-induced septic shock | Anti-inflammation | [68] |
|