Pregnancy-specific glycoprotein 1 (PSG1) activates TGF-β and prevents dextran sodium sulfate (DSS)-induced colitis in mice.
Pregnancy-specific glycoprotein 1 (PSG1) activates TGF-β and prevents dextran sodium sulfate (DSS)-induced colitis in mice.
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转化生长因子β（TGF-βs）作为潜在复合物从细胞分泌，并且TGF-βs的活性主要通过这些复合物的活化来控制。对胎儿同种异体移植物的耐受是妊娠成功的关键; TGF-β1和-β2在调节这些过程中起重要作用。妊娠特异性β-糖蛋白（PSG）在整个妊娠期间以高浓度存在于母体循环中，并已被认为具有抗炎功能。我们发现重组和天然PSG 1在体外激活TGF-β1和TGF-β2。与这些发现一致，给予PSG 1保护小鼠免受DSS诱导的结肠炎，减少促炎细胞因子的分泌，并增加调节性T细胞的数量。PSG 1介导的保护作用被中和性抗TGF-β Ab联合给药大大抑制。我们的研究结果表明，胎盘分泌的蛋白质直接有助于活性TGF-β的产生，并将PSG 1鉴定为少数已知的TGF-β2生物激活剂之一。
Transforming growth factor beta (TGF-βs) are secreted from cells as latent complexes and the activity of TGF-βs is controlled predominantly through activation of these complexes. Tolerance to the fetal allograft is essential for pregnancy success; TGF-β1 and -β2 play important roles in regulating these processes. Pregnancy-specific β-glycoproteins (PSGs) are present in the maternal circulation at high concentration throughout pregnancy and have been proposed to have anti-inflammatory functions. We found that recombinant and native PSG1 activate TGF-β1 and TGF-β2 in vitro. Consistent with these findings, administration of PSG1 protected mice from DSS-induced colitis, reduced the secretion of pro-inflammatory cytokines and increased the number of T regulatory cells. The PSG1-mediated protection was greatly inhibited by the co-administration of neutralizing anti-TGF-β Ab. Our results indicate that proteins secreted by the placenta directly contribute to the generation of active TGF-β and identify PSG1 as one of the few known biological activators of TGF-β2.
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