Table 2.

Genetically modified mice with altered phenotypes of apoptotic-cell clearance

	Defect
Genetic modification	in vivo	in vitro	Tissue / cell affected	Autoimmunity	Refs
C1qa–/–	Yes	Yes	Kidney, peritoneal macrophage	Increased antihistone,ANA antibodies,glomerulonephritis	105,110
C4–/–	Yes	NT	Elicited peritoneal macrophage	NT	110
CD93–/–	Yes	No	Elicited peritoneal macrophage	Normal	122
SR-A–/–	No	Yes	ND	NT	107
ABCA1–/–			Embryonic footplate, elicitedperitoneal macrophage	Glomerulonephritis	106,123
PU.1–/–	Yes	NT	Embryonic footplate, macrophage	NT	21
merkd	Yes		Thymus (induced apoptosis),elicited peritoneal macrophage	Increased antichromatin,anti-DNA, anti-IgGantibodies, mild renalpathology	108,111
TGase2–/–	Yes	Yes	Thymus (induced apoptosis),liver (induced apoptosis),peritoneal macrophage, Kupffercell	Increased autoantibodies,glomerulonephritis	76
Gal3–/–	Yes	Yes	Elicited peritoneal macrophage.Phagocytic defect not restrictedto apoptotic cells	NT	124
PSR–/–	Yes	Yes	Developing lung and brain, fetalliver, elicited peritonealmacrophage	NT	109,125
MFG-E8–/–	Yes	Yes	Lymphoid, tingible bodymacrophage, elicited peritoneal macrophage	Late-onset increased anti-dsDNA, antinuclearantibodies,glomerulonephritis	53
CD14–/–	Yes	Yes	Primary and secondary lymphoid,lung, liver, gut, peritonealmacrophage, bone marrowmacrophage	Normal	Devitt, Gregory et al., submitted

Gal-3^–/–, galectin-3 deficient; mer^kd, kinase-defective mutant of mer; ND, none detected; NT, not tested; SR-A, scavenger receptor-A; TGase2, tissue transglutaminase. See Fig. 1 for other abbreviations.