Abstract

Pregnancy is a phenomenon of natural transplantation, because the extraembryonic membranes, as well as the embryo, express the histocompatibility antigens of father’s haplotype and may serve as a potential target for the immunocompetent mother’s cells [7, 8]. The main hormone of pregnancy, chorionic gonadotrophin (CG), is synthesized by the placenta. It regulates the growth and development of the fetoplacental complex beginning from the ovum implantation until the birth [1]. It is known that this hormone not only exerts an independent immunomodulating effect, but also mediates it due to steroidogenesis induction. The latter evokes oppositely directed effects, the mode of which (positive or negative) is determined by the CG concentration and the stage of differentiation of the immunocompetent cells [2, 5]. The reactivity of the immune system of the mother during pregnancy is controlled by the fetoplacental unit. In the course of this control, positive (immunotrophic) effects are selected, whereas unfavorable (cytotoxic) effects are prevented. During pregnancy, the potential of cell-mediated responses determining the processes of the transplant rejection decreases, whereas the possibility of the realization of humoral responses increases [4, 6, 11]. Because the immune response represents an integrated reaction of the organism to the effects of various antigens, the purpose of this work was to study the CG effect on the immune-response polarization towards the cell-mediated or humoral responses. The experiments were performed on mature female Swiss mice weighing 20‐22 g. The animals were divided into three groups. Group I animals (control) were injected with the CG solvent. The other two groups received subcutaneous injections (every other day) of CG at two concentrations, which were extrapolated from the average hormone concentrations in blood serum of pregnant women in the I and II‐III trimesters (200 and 20 IU per mouse, respectively) [11]. To estimate the effect of CG on certain stages of the development of humoral and cell-mediated immune response, we performed three series of experiments. In series I, we studied the hormone effect on the antigenindependent stage of the immune response. For this purpose, the mice were administered with CG for five days prior to immunization (three injections). In series II, we studied the effect of the hormone on the antigendependent stage of the immune response. In this case, the hormone was injected according to the same scheme immediately after immunization. In series III, we studied the effect of the hormone on the antigendependent and antigen-independent stages of the immune response. The hormone was injected both before and after immunization (five injections during 10 days in total). In all three schemes, the humoral and cell-mediated immune response were estimated simultaneously. For this purpose, the mice were intraperitoneally immunized with sheep erythrocytes (SE) at a dose of 10 8 cells. Four days after the immunization, a resolving dose of SE (5 〈 10 7 cells) was injected into the foot to induce the delayed-type hypersensitivity (DTH). Twenty-four hours after this injection, the animals were withdrawn from the experiment, and the DTH response and the number of the antibody-forming cells (AFCs) in the spleen were evaluated. The DTH response was estimated by measuring the size of the foot edema in comparison with the intact foot. The difference in its thickness, expressed in millimeters, characterized the DTH response expression [10]. The AFC level was determined directly by local hemolysis in agarose gel according to Jerne [9].

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