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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >VIP boosts regulatory T cell induction by trophoblast cells in an in vitro model of trophoblast-maternal leukocyte interaction
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VIP boosts regulatory T cell induction by trophoblast cells in an in vitro model of trophoblast-maternal leukocyte interaction

机译：VIP在滋养层细胞与母体白细胞相互作用的体外模型中促进滋养层细胞对调节性T细胞的诱导

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摘要

Inducible regulatory T cells (Tregs) exert a timely and efficient immunosuppressive action at the critical peri-implantation stage essential for maternal tolerance to the conceptus. Vasoactive intestinal peptide (VIP) promotes anti-inflammatory and tolerogenic profiles through binding to VIP receptors on immune cells. We evaluated whether VIP produced by trophoblast cells induces Tregs during the early interaction of maternal leukocytes with trophoblast cells, thus contributing to maternal tolerance. We used an in vitro model of maternal leukocyte-trophoblast cell interaction represented by cocultures of fertile women's PBMCs with a human trophoblast cell line (Swan-71) and evaluated the effect of VIP added exogenously and of the endogenous polypeptide. VIP increased the frequency of CD4(+)CD25(+)FoxP3(+) cells after coculture, and these cells were able to suppress the maternal alloresponse. VIP also increased the frequency of CD4(+)IL10(+) and CD4(+)TGF beta(+) cells, but it did not modulate IFN-gamma or IL-17 production. Swan-71 secreted VIP, and their coculture with maternal PBMCs significantly increased the frequency of Tregs. This effect was even more pronounced if the trophoblast cells had been pretreated with VIP. In both situations, the VIP antagonist prevented the increase in the frequency of CD4(+)Foxp3(+) cells, reflecting a specific effect of the polypeptide after the interaction with Swan-71 cells. Finally, the increase in CD4(+)CD25(+)FoxP3(+) frequency was prevented by an anti-TGF-beta Ab and a VIP antagonist. These results suggest that VIP could have an active role in the immunoregulatory processes operating in the maternal-placental interface by contributing to the induction of Tregs through a mechanism involving TGF-beta 1.
机译：诱导型调节性T细胞（Tregs）在关键的围植入期对母体对概念的耐受至关重要，可发挥及时有效的免疫抑制作用。血管活性肠肽（VIP）通过与免疫细胞上的VIP受体结合来促进抗炎和致耐受性。我们评估了由滋养层细胞产生的VIP是否在母体白细胞与滋养层细胞的早期相互作用期间诱导Treg，从而促进了母体的耐受性。我们使用了以可育女性PBMC与人类滋养层细胞系（Swan-71）共同培养为代表的母体白细胞-滋养层细胞相互作用的体外模型，并评估了外源添加VIP和内源多肽的效果。共培养后，VIP增加了CD4（+）CD25（+）FoxP3（+）细胞的频率，这些细胞能够抑制母体的过敏反应。 VIP还增加了CD4（+）IL10（+）和CD4（+）TGF beta（+）细胞的频率，但它不调节IFN-γ或IL-17的产生。 Swan-71分泌VIP，并且它们与母体PBMC的共培养显着增加了Treg的频率。如果用VIP预处理了滋养层细胞，则这种作用更加明显。在这两种情况下，VIP拮抗剂均能阻止CD4（+）Foxp3（+）细胞频率的增加，反映出该多肽与Swan-71细胞相互作用后的特定作用。最后，抗TGF-βAb和VIP拮抗剂可阻止CD4（+）CD25（+）FoxP3（+）频率的增加。这些结果表明，VIP通过参与TGF-beta 1的机制促进Tregs的诱导，可能在母体-胎盘界面的免疫调节过程中发挥积极作用。

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