ABSTRACT
We studied the action of cytotrophoblast cells (CTC) on the expression of T lymphocyte membrane markers in the cultures of newborn cord blood mononuclear cells (CBMC) and peripheral blood mononuclear cells (PBMC) of a pregnant woman. The CTC were separated from the placental chorion at ten weeks of gestation time. In this abstract we show that the CTC and the CTC culture supernatant (SN) increase the number of HLA DR(+)CD7(+) T cells activated by anti-CD3 mAbs, both in PBMC and CBMC cultures. CTC increased the number of transferrine receptor CD71(+) lymphocytes without anti-CD3 activation in CBMC cultures. The increase in the blood mononuclear cell proliferation did not come with an increase of HLA DR and CD71 expression induced by CTC or SN. Moreover, SN caused the suppression of activated T lymphocyte proliferation. We found no signs of any influence of CTC and SN on the expression of CD25 in CD4(+) and CD8(+) subpopulations of T lymphocytes, either activated or non-activated by anti-CD3. The data regarding the CTC- and SN-induced HLA DR expression in vitro suggest that the previously determined high level of HLA DR(+) T cells in the placenta and decidua in pregnant women might have been the result the activity of the trophoblast cells and their soluble products on the lymphocytes of that area.
Subject(s)
Fetal Blood , Leukocytes, Mononuclear , Antigens, Surface/pharmacology , Female , Fetal Blood/cytology , Humans , Infant, Newborn , Leukocytes, Mononuclear/drug effects , Lymphocyte Activation , Lymphocyte Function-Associated Antigen-1 , Lymphocyte Subsets/immunology , Pregnancy , T-Lymphocytes/immunology , Trophoblasts/immunologyABSTRACT
We have shown that the severity of newborns' clinical condition is accompanied by two independent deviations in functional properties of T cells: week proliferative response to activation through CD3 molecule and high sensitivity to apoptosis. Studies of effects exerted by recombinant interleukins and dexamethasone upon cord blood mononuclear cell (CBMC) apoptosis proves that the IL-2, -4 and -7 deficiency is common to enhance apoptosis in CBMC cultures of newborn infants. However, interleukin deficiency is not the sole cause of high level of CBMC apoptosis, and some other factors are required, which may determine the cell sensitivity towards apoptosis. The weakness of proliferative response of T cells to activation seems to be determined rather by the effect of suppressive factors, production of which can be blocked by dexamethasone, than by the death of activated cells in apoptosis.
