Strong prostaglandin associated suppression of the proliferation of human maternal lymphocytes by neonatal lymphocytes linked to T versus T cell interactions and differential PGE2 sensitivity.

Lymphocytes from human fetuses and newborns strongly, regularly, and non-specifically suppress the proliferation of PHA stimulated peripheral blood mononuclear leucocytes. The suppression is prostaglandin (PG)-dependent. Our present investigation clearly indicates that the suppression is associated with neonatal T versus maternal T lymphocyte interactions, independent of monocytes. This was borne out from co-cultures of PHA stimulated maternal and male cord T cells enriched by nylon wool columns (greater than 90% T3+ cells; residual adherent cells ranging between 0 and 0.05%, and sIg+ cells between 0.6 and 3.2%). Sex chromosomes served as markers for dividing cord (male) or maternal cells. Each of three separate PG synthetase inhibitors introduced into the co-cultures-indomethacin 28 microM, 5, 8, 11, 14-eicosatetraynoic acid (ETYA) 33 microM, or Naprosyn 217 microM--decreased the suppression of the maternal T cells by a maximum of 65%, indicating the importance of PG for the suppression. Moreover, exogenous PGE2 ranging between 1.4 X 10(-5) and 1.4 X 10(-9) M strongly suppressed the proliferation of PHA stimulated maternal T cells (ranging between 62 and 26%) but left the proliferation of cord T cells virtually unchanged. This difference offers one explanation for the strong and invariable suppression of adult lymphocytes by fetal/neonatal lymphocytes. The suppression might be of importance for prohibiting rejection of the placenta by maternal lymphocytes.