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.

摘要

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 fetaleonatal lymphocytes. The suppression might be of importance for prohibiting rejection of the placenta by maternal lymphocytes.