Table 5.

Dendritic cell defects in human primary cells and in the mouse model of STIM and ORAI deficiency

Gene	Manipulation	Ca2+ Signaling	Maturation/Differentiation	Cytokine Production	Phagocytosis	Ag Presentation	Ref. No.
Human dendritic cells
STIM1	siStim1, human blood-derived DC	Decreased 60% (Tg)	Decreased 30–50% (CD80, CD86, CD83, MHC-CII, in response to Tg, LPS, zymosan, TNF-α)				31
ORAI1	siOrai1, human blood-derived DC	Decreased 60% (Tg)	Decreased 30–50% (CD80, CD86, CD83, MHC-CII, in response to Tg, LPS, zymosan, TNF-α)				31

Gene	Mouse Model	Ca2+ Signaling	Maturation/Differentiation	Cytokine Production	Phagocytosis	Ag Presentation	Ref. No.
Mouse dendritic cells
Stim1 and Stim2	Vav-Cre Stim1−/−; Stim2−/− Myeloid ablation	Decreased >95% (Tg) Normal store content 20% decrease (ATP)	Normal (CD86, MHC-CII, in response to LPS, CpG, zymosan, curdlan, imiquimod)	Normal (IL-2, IL-6, IL-10, IL-12p40, IL-12p70, IL-23p19, TNF-α in response to LPS, CpG, zymosan, curdlan, imiquimod, IL-1b in response to ATP, FlaTox, MSU)	Normal (1:1, 1:5,1:25 unopsonized and IgG-coated beads)	Normal (OT-II CD4+ T cells co-cultured with BMDCs exposed to 500 μg/ml OVA)	117

The table lists the in vitro dendritic cell defects reported in human dendritic cells from peripheral blood and in the mouse model of Stim1 and Stim2 deficiency. BMDC, bone-marrow derived dendritic cell; OVA, ovalbumin.