A deficiency of placental IL-10 in preeclampsia

SAccommodation of the fetoplacental unit in human pregnancy requires matern al immune tolerance to this "semiallograft", Local antiplacental immunity i s modified by synthesis of uncommon histocompatibility Ags (e.g., HLA-G), g rowth factors, and cytokines by the placenta. Placental interleukins have b een identified in reproductive tissues, but their roles in adaptive materna l immunity and determining term pregnancy outcomes have not been fully clar ified. This study examined the distribution of IL-10 and TNF-a staining in term placentas. Women with proteinuric hypertension (PE, n = 10) were compa red with an age-matched group with normal pregnancy (NP, n = 14) and gestat ional hypertension (GH, n = 6), Using immunohistochemistry of parrafin-fixe d tissues, trophoblast cells were identified by cytokeratin 7 and cytokerat in 18 staining, The cytokine binding of villous trophoblast cells was score d depending on the extent of circumferential cytoplasm staining (<25%; inte rmediate or >75%), The cytokine positive decidual cells were scored as a pe rcentage of total extravillous trophoblast cells. There was a reduction in villous IL-10 immunostaining compared with normal term placenta (PE, 10.2 /- 1.1, mean +/- SEM; NP, 14.07 +/- 1.16 Mann-Whitney U test; p = 0.02), In these patients, there was an increase in TNF-alpha immunostaining, Sparse endovascular extravillous trophoblast cells demonstrated nuclear IL-10 stai ning in 30% of patients with preeclampsia, Serum IL-10 was diminished in wo men with preeclampsia compared with normal pregnancy. In conclusion, villou s trophoblast demonstrated diminished immunostaining of IL-10 in preeclamps ia, This abnormality may be associated with heightened maternal antifetal i mmunity and therefore inadequate placental development in preeclampsia.