Introduction

Pre-eclampsia only occurs during pregnancy, a physiological situation where allogeneic cells from two different individuals come into close contact. Furthermore, the development of the disease is dependent only on the presence of the placenta and not the fetus as the disease is frequently seen in complete hydatidiform mole where no fetus is present. Numerous epidemiological studies have given rise to the widely held view that immunological mechanisms probably contribute to the pathogenesis of this disease (and indeed other pregnancy disorders) (Dekker, 2002; Redman, 1991; Roberts and Lain, 2002; Walker, 2000). However, the molecular and biological mechanisms underlying this presumed maternal immune maladaptation remain unknown.

During pregnancy both the maternal and fetal immune systems would be expected to recognize the presence of each other's allogeneic cells. However, the acceptance of the fetal allograft by the mother is at variance with the rejection typically seen with organ grafts. If the transplant analogy is extended further it would be expected that the maternal immune reaction would exhibit both specificity and memory for particular paternal genes expressed by the placenta. In other words, is there a partner-specific effect which contributes to pregnancy success or failure? Therefore, in considering possible immunological factors in pre-eclampsia two broad questions arise: first, how does the maternal immune system normally allow a symbiotic relationship with the feto-placental unit and, second, can this symbiosis be altered in a partner-specific way in pre-eclampsia?