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Detection of antitrophoblast antibodies in the sera of patients with
anticardiolipin antibodies and fetal loss
KR McCrae, AM DeMichele, P Pandhi, MJ Balsai, P Samuels, C Graham, PK Lala and DB Cines
Department of Medicine, University of Pennsylvania School of Medicine,
Philadelphia.
Women with anticardiolipin antibodies (ACLA) are at increased risk for
fetal loss. One potential explanation for this outcome is that sera from
these individuals contain antibodies reactive with trophoblast cells, which
are involved in the establishment of the uteroplacental vasculature and
maintenance of placental blood fluidity. To examine this hypothesis, we
compared the incidence of trophoblast-reactive antibodies in 27 patients
with ACLA and a history of fetal loss with that in 29 normal pregnant
women. Sera from 20 patients, but only one control, contained
trophoblast-reactive antibodies (P < .001). These antibodies were not
directed against major histocompatibility class I antigens, and reacted
with both term and first-trimester trophoblast cells. In most cases, sera
from which ACLA were adsorbed by cardiolipin- containing liposomes
maintained reactivity against cells. In addition, patient Ig fractions
immunoprecipitated an approximately 62-kD protein from the trophoblast cell
surface, stimulated the release of arachidonic acid and thromboxane A2 by
trophoblasts, and inhibited the binding of prourokinase to trophoblast
urokinase receptors. These observations show that sera from women with ACLA
and a history of fetal loss contain antitrophoblast antibodies. These
antibodies may be serologically distinct from ACLA, and may contribute to
the pathogenesis of fetal demise.
Volume 82,
Issue 9,
pp. 2730-2741,
11/01/1993
Copyright © 1993 by The American Society of Hematology
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