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
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.
Sinkovics JG, Horvath JC. Role of Apoptosis in Health and Disease. JAMA. 1998;279(21):1699-1700. doi:10-1001/pubs.JAMA-ISSN-0098-7484-279-21-jbk0603