A transforming growth factor beta 2 (TGF-beta 2)-like immunosuppressive factor in amniotic fluid and localization of TGF-beta 2 mRNA in the pregnant uterus.
A transforming growth factor beta 2 (TGF-beta 2)-like immunosuppressive factor in amniotic fluid and localization of TGF-beta 2 mRNA in the pregnant uterus.
复制标题
羊水中的转化生长因子 β 2 (TGF-β 2) 样免疫抑制因子以及妊娠子宫中 TGF-β 2 mRNA 的定位。
DOI:
10.1084/jem.172.5.1391
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发表时间:
1990
期刊:
影响因子:
--
通讯作者:
Tomasi,TB
中科院分区:
文献类型:
--
作者:
Altman,DJ;Schneider,SL;Thompson,DA;Cheng,HL;Tomasi,TB
This report describes a murine amniotic fluid (MAF) immunosuppressive factor that has properties similar to transforming growth factor 0 (TGF-R). The MAP factor exhibits TGF-0-like activity in stimulating soft agar colony formation by AKR-2B cells and inhibiting thymidine uptake by Mv1Lu cells. We demonstrate that both the immunosuppressive and TGF-#-like activities ofthe MAP factor are completely neutralized by antiTGF-02-specific antibodies and not by anti-TGF-/31-specific antisera. The immunosuppressive factor in MAP is novel in that it appears to be identical or very closely related to TGF-02 and is active in its native state. This active and antiTGF-, 32-neutralizable factor chromatography at-70 kD on Sephadex at neutral pH and appears to be able to complex with ci-fetoprotein in native amniotic fluid. Chromatography of native MAP under acidic conditions demonstrates a lower molecular mass protein that chromatographs on BioGel in the same position as the mature 25-kD TGF-0. This protein has the biological properties of TGF-O and is immunosuppressive. Both of these activities are neutralizable with antiTGF-/32 but not with antiTGF-/31 or other antisera. By Northern analysis, we find high levels of TGF-f2 mRNA (with little or no TGF-fl) in the pregnant uterus that peak around day 15 of gestation and then fall rapidly by day 19 as birth approaches. The TGF-X32-like factor could possibly play a role in maternal immunity, in the retention of the fetal allograft, as well as in regulating fetal and neonatal immunological competence.Several factors have been implicated in the maternal tolerance to the semiallogeneic fetus and the immunological deficiencies described in pregnancy, as well as the fetus and neonate (reviewed in references 1 and 2). This includes evidence that deficiencies in MHC class I and class II antigen expression on fetal and maternal tissues may play a role in maternal tolerance. Different T cell subsets and especially suppressor cells have also been implicated in pregnancy-related immune suppression and in the immunotrophic promotion offetal development (1, 2). Neonatal natural suppressor cells inhibit immune responses and may be involved in tolerance induction in the fetal and neonatal periods (3). In addition, soluble suppressive factors influencing immune development in the fetus and newborn, and immunity during pregnancy, have been described (1), and these may mediate and/or complement the cellular suppressors. We have previously reported (reviewed in references 4 and 5) the immunosuppressive effects of murine amniotic fluid