Strong association between the responder status of the FC gamma II receptor and recurrent spontaneous abortion.

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 FcgammaII receptor (FcgammaIIR) in RSA was suggested, since FcgammaIIR-blocking antibodies, present in normal pregnancies, could not be found in patients suffering from RSA. The FcgammaIIR 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 FcgammaIIR 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 less than or equal to 0.0001). Our results suggest further that the FcgammaIIR dimorphism might be involved in the pathogenesis of RSA.