Other experts say the findings could have important implications for work on transplants.

When patients receive transplanted organs, they generally have to take drugs to suppress their immune system and keep it from attacking the foreign tissue. But these drugs may be associated with greater susceptibility to kidney problems, infection and bone weakness, said Dr. Burlingham, of Wisconsin.

“We would like to find ways of transplanting tissue without creating lifelong dependence on these drugs,” he said. “That might be possible if researchers took the immune profiles of patients’ mothers into account to a great degree when selecting organs for transplant.”

As early as the 1980s, scientists in the Netherlands observed that many patients who were waiting to receive kidney transplants and who had formed antibodies against most potential donors did not react against their own mothers’ white blood cells. That suggested that during fetal development, a process was allowing the fetus to tolerate tissue with motherlike surface molecules.

The new research explains “precisely how that works,” said Dr. Jon J. van Rood, a professor of internal medicine at the University of Leiden who conducted the original research. By homing in on regulatory T cells in fetal lymph nodes, “they found the crucial clue.”

The discovery may also be relevant to the study of mother-to-child transmission of infectious disease.

When pregnant women are infected with H.I.V., for instance, they often do not pass the disease to the fetus, said Dr. Joseph M. McCune, the immunologist who led the U.C.S.F. group. Fewer than half of all babies born to H.I.V.-positive mothers are infected themselves, and of those, only a small fraction are infected in the womb, he said.

If H.I.V. is crossing the placenta in the same way as the mother’s cells and if the fetus is also suppressing an immune response against the virus, it is surprising that more fetuses are not infected, he said.