Table 2: C5aR2 KO on C57BL/6 background.

SourceDisease modelProperties of C5aR2Refs

B. Lu, Harvard Medical
School, USA
IC-induced acute lung injuryAnti-inflammation[34]
Anti-mMPO-induced ANCA
CLP-induced sepsis and in vitro
assays on leukocytes
Proinflammation and indispensable
for HMGB-1 release
CLP-induced sepsisOn CMs—proinflammation
and causes cardiac dysfunction
[75, 76, 78]
Acute pyelonephritisProinflammation[72]
Renal I/R injuryProinflammation[73]
Experimental cerebral malariaNo function[124]
S. aureus bloodstream infectionAnti-inflammation[125]
AKI induced by LPS, IC, or C5aProinflammation[71]
Genotyping and breeding
in University of Michigan
according to the method
of Dr. Craig Gerard
CLP-induced sepsisIndispensable for G-CSF release by macrophages[79]
CLP-induced sepsisOn CMs—proinflammation:
activation of the cardiac NLRP3 inflammasome
Professor A. Klos, Hannover Medical School, GermanyWire-induced endothelial denudation of the carotid artery, diet-induced atherosclerosisProinflammation[66]
The Jackson LaboratoryIn vitro atherosclerosis modelOn PBMCs and BMDMs—proinflammation[87]
Lexicon Genetics, the Woodlands, TexasThioglycollate-induced peritonitis
and air-pouch inflammation
‚ÄČLPS-induced septic shockAnti-inflammation[68]

※ means that C5a-C5aR1 contributes to the cerebral [124] and placental [126] malaria pathogenesis in human and mouse, rather than to C5a-C5aR2 signal.