| Abstrakt: |
Successful pregnancy is associated with maternal immune sensitization to placental antigens. Placental trophoblast cells at the maternal-fetal interface express histocompatibility antigens of both the maternal and paternal haplotypes. In particular, these paternal-type antigens have the potential to stimulate alloreactive maternal immune responses and, as a result, maternal T cells appear in the decidua shortly after class I major histocompatibility complex encoded antigens are expressed. Despite this maternal immune recognition, immunologic destruction of the fetus rarely occurs. In fact, recent evidence suggests that the interaction between maternal T cells and placental cells results in an "immunotrophic" effect that stimulates placental growth and fetal survival. To better understand the contribution of fetally derived placental cells in the activation of maternal immunity, we have developed a murine lymphokine-dependent long-term placental cell line termed "FRD." FRD cells can stimulate syngeneic, semi-syngeneic, and allogeneic murine spleen cells to proliferate in a mixed lymphocyte-placental cell reaction. Coculture experiments with T hybridomas show that unlike conventional antigen-presenting cells, FRD can activate T cells to secrete lymphokines in the absence of specific antigen. In addition, lymphokine-activated FRD cells release factors that directly stimulate proliferation of the IL 1 responsive T cell line D10.G4.1. These observations suggest that placental cells stimulate T cells via novel mechanisms that may play a role in producing a maternal T cell response that in turn is beneficial to fetally derived tissues during pregnancy. |
