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Table I.

Crry-Ig Specifically Prevents aPL Antibody-induced Fetal Resorption and Growth Retardation


Human IgG source:

aPL

aPL

Cntrl IgG

Cntrl IgG
Mouse reagent:
mIgG
Crry-Ig
mIgG
Crry-Ig
Number of mice 11 14 10 11 
Frequency of fetal resorption 0.29 ± 0.09a 0.08 ± 0.03 0.10 ± 0.05 0.08 ± 0.03 
Fetal weight (mg)
 
171 ± 27a
 
256 ± 38
 
273 ± 32
 
281 ± 34
 

Human IgG source:

aPL

aPL

Cntrl IgG

Cntrl IgG
Mouse reagent:
mIgG
Crry-Ig
mIgG
Crry-Ig
Number of mice 11 14 10 11 
Frequency of fetal resorption 0.29 ± 0.09a 0.08 ± 0.03 0.10 ± 0.05 0.08 ± 0.03 
Fetal weight (mg)
 
171 ± 27a
 
256 ± 38
 
273 ± 32
 
281 ± 34
 

Female BALB/c mice were given aPL-IgG (10 mg) or normal human IgG (Cntrl IgG) (10 mg) intraperitoneally on days 8 and 12 of pregnancy. Mice also received either Crry-Ig (3 mg) or polyclonal murine IgG (mIgG) (3 mg) intraperitoneally every other day from days 8–12. Mice were killed on day 15 of pregnancy, uteri were dissected, fetuses were weighed, and frequency of fetal resorption calculated (number of resorptions/number of fetuses plus number of resorptions). Treatment with aPL-IgG caused an increase in fetal resorptions and a decrease in fetal weight (aaPL plus mIgG versus Cntrl IgG plus mIgG; P < 0.001) which was prevented by Crry-Ig (aaPL plus mIgG versus aPL plus Crry-Ig; P < 0.001). Treatment with mIgG did not affect either pregnancy outcome.

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