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STRONG ASSOCIATION BETWEEN THE RESPONDER STATUS OF THE FCγ II RECEPTOR and RECURRENT SPONTANEOUS ABORTION
Author(s) -
Lorenz A.,
Blasczyk R.,
Kuhn U.,
Venjakob U.,
Mendonca M.,
GrosseWilde H.
Publication year - 1995
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1995.tb00254.x
Subject(s) - abortion , immunology , fetus , receptor , pregnancy , antibody , medicine , biology , genetics
SUMMARY Several models exist for the aetiology and therapy of recurrent spontaneous abortion (RSA). They are based in part on the assumption that an increased materno‐fetal histocompatibility results in an insufficient maternal immunological recognition of the fetus, and thus renders the maternal immune system unable to sustain the pregnancy. The involvement of the FCγII receptor (FcγIIR) in RSA was suggested, since FcγIIR‐blocking antibodies, present in normal pregnancies, could not be found in patients suffering from RSA. The FcγIIR is known to be functionally and structurally dimorphic, which results in a responder, respectively non‐responder pattern. We used an in vitro proliferation assay to distinguish between FCγIIR responder and non‐responder phenotypes. In 29 RSA couples we found 97% (28/29) of RSA patients and 100% (29/29) of their partners to be responders, whereas 50 fertile couples and a further 100 unrelated controls revealed distributions of responder vs. non‐responder of 73% vs. 27% and 70% vs. 30%, respectively. These differences (RSA vs. controls) are highly significant ( P ≤ 0.0001). Our results suggest further that the FcγIIR dimorphism might be involved in the pathogenesis of RSA.