Abstracts
285
occurs in chickens and rabbits respectively, and switching to downstream constant regions probably occurs in utero, even in the theoretical absence of environmental antigens and maternal regulatory molecules. Preferential V(H)A expression is probably a selection phenomenon.
Regulation of fetal allograft survival by hormone-controlled type cytokines
Piccinni M.-P., Romagnani Istituto
di Medicina
[Immunologic
Thl-
and Th2-
S.
Interna, Immunoallergologia,
Viale Morgagni
85. I-50134
Firenze, Italy
Research 15(2), 141- 150; 19961
There is clear evidence to suggest that the maternal immune system during pregnancy can enhance or inhibit the development of the fetoplacental unit. Recent data support the view that some cytokines produced by both T cells and non-T cells (IL-3, GM-CSF, TGF-beta, IL-4, IL-lo), favor fetal survival and growth. In contrast, other cytokines, such as IFN-gamma, TNF-beta and TNF-alpha, can rather compromise pregnancy. Accordingly, we show here that T-cell clones generated from the decidua of women with unexplained recurrent abortion produced significantly lower concentrations of IL-4 than clones derived from the decidua of voluntary abortions or the endometrium of nonpregnant women. Thus, despite the complexity of the cytokine network, it appears that cytokines favoring the maintenance of fetal survival mainly belong to the Th2 pathway, whereas the failure of pregnancy rather associates with the predominance of Thl-type cytokines and/or the absence of ThZtype cytokines. Interestingly, we also found that, at least in vitro, progesterone promotes the preferential development of Th2-like cells and induces transient IL-4 production by established Thl cells, whereas relaxin, another corpus luteum-derived hormone, mainly promotes the development of Thl-like cells. These data provide an excellent basis for investigating the relationship between the endocrine and the immune system in the regulation of the maternal-fetal interaction.
Immunmodulating
cytokines
induce term and preterm parturition
Steinborn A., Kuhnert M., Halberstadt Department Obstetrics and Gynecology, 60590 Frankfurt, Germany
E.
University
qf Frunkfirt,
[Journal of Perinatal Medicine 24(4), 381-390;
Theodor-Stem-Kai
1. D-
19961
The aim of our study was to investigate if cytokines, which are able to cause preterm delivery in case of intraamniotic infection, also participate in
286
Absrract3
the mechanisms of normal term labor. Therefore, we estimated cytokine concentrations in cercicovaginal secretions of 96 patients, divided into four different collectives. In collective A (women with spontaneous term labor) cytokine concentrations raised from a median level of 278 pg/ml for Il-lbeta and 263 pg/ml for 11-6 in early term labor to a median level of 3351 pg/ml for 11-l beta and 39442 pg/ml for 11-6 at complete cervical dilatation. TNF-alpha-exclusively appeared after spontaneous rupture of fetal membranes. In collective B and C (women with preterm rupture of fetal membranes) cytokine concentrations declined from a maximum level of 1425 pg/ml for TNF-alpha, 12982 pg/ml for Il-lbeta and 29727 pg/ml for 11-6 soon after preterm rupture of membranes to a minimum level of 93 pg/ml for TNF-alpha, 851 pg/ml for 11-l beta and 780 pg/ml for 11-6 with remission of labor in case of successful tocolytic treatment. High concentrations reappeared with the onset of labor, unresponsive to tocolysis. In collective D (women with intact membranes) TNF-alpha was not detectable and 11-l beta and 11-6 appeared exclusively in the presence of labor. Our results suggest, that normal term labor may be controlled by biochemical processes, similar to infection-associated signal transduction, which is commonly accepted to induce preterm labor.
Changes in NK activities and TGF-beta concentration in the peritoneal cavity in endometriosis and their interaction related with infertility Mizumoto Y. Depurtmerlt of Obstetrics/Gynecology, Nutiorlal Defence Medical College, Saitama, Japan
[Acta Obstetrica
et Gynaecologica
Japonica
48(6), 379-385;
19961
The purpose of this study was to clarify the relationship between NK activity and TGF-beta in the immune system in endometriosis. We investigated (1) the changes in the NK activity and concentration of TGF-beta in human peritoneal fluid (HPF), and (2) the effects of HPF and TGF-beta on the development of early mice embryos. In a rat model of experiment endometriosis. we observed the effects of tissue culture supernatants of peritoneum on NK activity in rat cells, and obtained the following results. (1) NK activity of peripheral lymphocytes in healthy women was significantly suppressed in the presence of HPF of endometriosis. (2) The concentrations of TGF-beta significantly higher in HPF of endometriosis than in HPF of healthy women. (3) Both HPF of endometriosis and TGF-beta significantly inhibited the development of early mice embryos. (4) The supernatants prepared from the intact peritoneum of the rat model showed marked inhibition of NK activity compared to control rats, although the peritoneum was obtained from a region distant from the implanted en-