Murine experimental abortion by IL-2 administration is caused by activation of cytotoxic T lymphocytes and placental apoptosis.

Objective: Fetal loss caused by IL-2 administration to pregnant mice is regarded as a model of human habitual abortion due to allo-immune reactions. To estimate feto-placental damages in this model, we examined apoptosis histochemically in the placenta.

Methods: Four allogenic mated mice were administered intraperitoneally with 1000 IU of recombinant human IL-2 on days 3, 5 (7) after mating. We examined the presence of apoptosis in the placentae by TUNEL stain. We also examined expression of CTL specific granzyme B/perforin mRNA and usage of TCR V beta receptor segments by RT-PCR.

Results: 1. Allogenic pregnant mice given IL-2 revealed increased apoptotic scores in villous trophoblasts compared with control mice. Extracted DNA from IL-2 treated placentae revealed ladder formations. 2. Expression of granzyme B mRNA was increased while expression of perforin mRNA was not changed. 3. We observed increased numbers of TCR V beta gene segments in the decidua from IL-2 treated mice compared with untreated mice.

Conclusion: We suggest that placental apoptosis caused by activation of maternal CTL may play important roles in the rejection of fetal allografts.