Role of PIR-B in Autoimmune Glomerulonephritis

Table 1

Phenotypes observed in Pirb^−/− mice and Pirb transgenic (tg) mice.

Mice	Cellsa	Phenotypesb	References
Pirb ^-/-	B-2 cells	Enhanced proliferation upon BCR stimulation	[10]
	B-1 cells	Enhanced proliferation and autoantibody production upon CpG stimulation	[11]
	DCs	Impaired maturation	[10]
		Exacerbated graft-versus-host disease	[12]
	CD8^+ T cells	Augmented activation	[13]
	Mast cells	Augmented anaphylaxis	[14]
	Macrophages	Augmented cytokine and chemokine signaling	[15]
	Neutrophils	Augmented integrin signaling	[16]
	Eosinophils	Enhanced recruitment in Th2 response	[17]
	Macrophagesc	Sensitive to Salmonella infection	[18]
	Macrophages	Reduced binding of Staphylococcus aureus	[19]
	Neuronal cells	Enhanced plasticity of visual nerve connections	[20]
		Enhanced neurite outgrowth	[21]
Pirb tg	Thymocytes	Normal development	[22]
	Mature T cells	Impaired Th1 response	[22]

aCells involved mainly in the observed phenotype.
bMajor phenotypes observed.
cUnidentified, though involving macrophages.