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June 3, 1998

Role of Apoptosis in Health and Disease

Author Affiliations

Margaret A.WinkerMD, Senior EditorIndividualAuthorPhil B.FontanarosaMD, Senior EditorIndividualAuthor


Copyright 1998 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1998

JAMA. 1998;279(21):1699-1700. doi:10-1001/pubs.JAMA-ISSN-0098-7484-279-21-jbk0603

To the Editor.—In his article on apoptosis, Mr Hetts1addresses the FasL death ligand that binds to the death receptor Fas (FasR), beginning the apoptotic cascade. To our knowledge, the Good Institute2was 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.3We have proposed that enhancing antibodies (immune globulins that stimulate cell divisions)4 and suppressor cells (lymphocytes that antagonize a specific immune reaction)5coevolved 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 FasL→FasR system, as described in Hetts' article, was essential in the evolution of the placenta. Without this system there could be no mammals.

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