Interleukin-33 (IL-33) is a mucosal alarmin belonging to the IL-1 cytokine family and is now recognized to have a key role in innate and adaptive immunity, contributing to tissue homeostasis and response to environmental stresses. In addition, IL-33 has also been shown to work as a positive regulator that initiates and maintains a Th2 immune response. In the context of pregnancy, it has been recently demonstrated that upon certain stress conditions, such as an infection induced inflammation, IL-33 is released from the uterine mucosa and triggers decidual B cells to produce anti-inflammatory molecules, which in turn restore immune homeostasis and prevents the development of preterm birth. In this study we therefore performed a detailed characterization of IL-33 receptor (Il1rl1 or ST2) expression in B cells during normal pregnancy, as well as in a mouse model of preterm birth. We observed that splenic B cells significantly up-regulate the expression of Il1rl1 during pregnancy and identified the B1 B cell population as the main ST2-expressing B cell subset. A further kinetic analysis showed that percentages of ST2-expressing B1 B cells are significantly augmented on days 12 and 14 of pregnancy, both in the spleen and peritoneal cavity of pregnant mice, and then drop toward the end of pregnancy to the levels observed in non-pregnant animals. Furthermore, using a mouse model of LPS-induced preterm birth, we demonstrated that not only are the percentages of ST2-expressing B1 B cells significantly enlarged in the spleen during the acute phase of preterm birth, but decidual B cells also significantly up-regulate ST2 expression as compared to term-pregnant mice. Overall, our results suggest a functional role of ST2 expression in B cells during pregnancy and reinforce the importance of the IL-33/ST2 axis in B cells as a critical mechanism to control inflammation-induced preterm birth.

中文翻译：

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IL-33受体的表达在妊娠期间和小鼠早产急性期的B细胞中明显上调。

白介素33（IL-33）是属于IL-1细胞因子家族的粘膜警报蛋白，现已被认为在先天和适应性免疫中起关键作用，有助于组织体内稳态和对环境压力的响应。此外，IL-33还显示出可作为启动并维持Th2免疫应答的阳性调节剂。在怀孕的背景下，最近已证明，在某些压力条件下，例如感染引起的炎症，IL-33从子宫粘膜释放并触发蜕膜B细胞产生抗炎分子，进而恢复免疫力。体内平衡并阻止早产的发展。因此，在这项研究中，我们对正常怀孕期间B细胞中IL-33受体（Il1rl1或ST2）的表达进行了详细的表征，以及早产小鼠模型。我们观察到脾脏B细胞在怀孕期间显着上调Il1rl1的表达，并将B1 B细胞群体确定为主要表达ST2的B细胞亚群。进一步的动力学分析表明，在怀孕的第12天和第14天，怀孕小鼠的脾脏和腹膜腔中，表达ST2的B1 B细胞的百分比均显着增加，然后在怀孕结束时下降至在非小鼠中观察到的水平。 -怀孕的动物。此外，使用LPS诱导的早产小鼠模型，我们证明，不仅早产急性期脾脏中表达ST2的B1 B细胞百分比显着增加，而且蜕膜B细胞也显着上调与足月妊娠小鼠相比，ST2表达。总体，