Abstract
Mouse trisomy 16 is a well-studied model for human chromosome 21 trisomy (Down's syndrome). The late stage trisomy 16 mouse fetus exhibits significant growth retardation, inappropriately opened eyes, and convex rather than concave back curvature. The interferons (alpha, beta, and gamma) have potent growth retarding activity, and sensitivity to these cytokines is controlled by genes that map to mouse chromosome 16 and human chromosome 21. In experiments designed to determine if the interferons induce or aggravate the trisomy phenotype, mice pregnant with trisomy 16 fetuses were injected with a combination of anti-alpha, -beta, and -gamma interferon IgG. This maternal anti-interferon treatment was found to provide measurable benefit to the development and growth of the trisomic fetuses with significant return-toward-normal values observed for overall fetal growth, eye opening, and back curvature.
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