A mother readily rejects organ transplants from her offspring. Owing to the contribution of paternal genes, her child's tissues express different antigens to her own — and that's what gets her immune system going. Yet she carries these genetically disparate fetuses to term. What protects a fetus from attack by its mother's immune system? Reporting in Science (281, 1191-1193; 1998), Andrew Mellor and colleagues propose that, in mice, rapid consumption of the amino acid tryptophan at the maternal-fetal interface paralyses the mother's aggressive T cells.

Credit: PETIT FORMAT/NESTLE/SPL

Early in pregnancy, placental cells seem to synthesize indoleamine 2,3-dioxygenase (IDO), an enzyme that degrades tryptophan and can suppress T-cell activity in vitro. Pregnant mice exposed to an IDO inhibitor rapidly aborted their fetuses, unless the embryos were a result of inbreeding and, thus, had a similar genetic make-up to their mothers.

The inhibitor had no effect in mice lacking B and T cells, but when the females were supplemented with T cells their sensitivity to the inhibitor was restored and their pregnancies terminated. So, maternal T cells, directly or indirectly, mediate fetal rejection if they are not kept in check by IDO. Although it is not clear whether exhaustion of the tryptophan supply, or an obscure property of IDO, numbs the maternal T cells, it looks as though mothers do not reject their young because they're IDOlized from the start.