. 2017 Jun 15;2017:8193932. doi: 10.1155/2017/8193932

Table 2.

C5aR2 KO on C57BL/6 background.

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]

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