This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on ISI (6)  • Contact me when this article is cited  Related Content  • Similar articles in JAMA

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

To the Editor.—In his article on apoptosis, Mr Hetts¹ addresses the FasL death ligand that binds to the death receptor Fas (FasR), beginning the apoptotic cascade. To our knowledge, the Good Institute² was the first to provide data on placental FasL⁺ trophoblasts that endow the fetus with immunologically privileged status by eliminating FasR⁺ maternal lymphocytes, the lymphocytes aimed to attack fetal cells expressing paternal antigens. This seminal observation has been confirmed.³ We have proposed that enhancing antibodies (immune globulins that stimulate cell divisions)⁴ and suppressor cells (lymphocytes that antagonize a specific immune reaction)⁵ coevolved with the placenta. Placentation could not have established itself in the early Cenozoic era, the era when mammals began to outpopulate dinosaurs, without some compromise to the immune system. We believe that the FasLFasR system, as described in Hetts' article, was essential in the evolution of the placenta. Without this system there could be . . . [Full Text of this Article]