Maternal IgE activates fetal mast cells Mast cells (MCs) are immune cells that participate in allergic reactions through their activation by immunoglobulin E (IgE) antibodies. MCs arise early during mammalian development, but it is unclear whether IgE-mediated activation occurs in fetal tissues and what the source of IgE stimulation is. Msallam et al. show that human and mouse fetal MCs can be sensitized by IgE of maternal origin, which crosses the placental barrier through the fetal neonatal Fc receptor (see the Perspective by Rothenberg). Prenatal maternal sensitization conferred transient allergen sensitivity after birth and resulted in the development of postnatal skin and airway inflammation in the offspring after their first exposure to allergen. Thus, both maternal IgE and fetal MCs may influence mother-to-child transmission of allergic disease during gestation. Science, this issue p. 941; see also p. 907 Maternally derived immunoglobulin E can predispose offspring for allergic disease in neonatal and early life upon allergen exposure. Mast cells (MCs) are central effector cells in allergic reactions that are often mediated by immunoglobulin E (IgE). Allergies commonly start at an early age, and both MCs and IgE are detectable in fetuses. However, the origin of fetal IgE and whether fetal MCs can degranulate in response to IgE-dependent activation are presently unknown. Here, we show that human and mouse fetal MCs phenotypically mature through pregnancy and can be sensitized by maternal IgE. IgE crossed the placenta, dependent on the fetal neonatal Fc receptor (FcRN), and sensitized fetal MCs for allergen-specific degranulation. Both passive and active prenatal sensitization conferred allergen sensitivity, resulting in postnatal skin and airway inflammation after the first allergen encounter. We report a role for MCs within the developing fetus and demonstrate that fetal MCs may contribute to antigen-specific vertical transmission of allergic disease.

中文翻译：

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胎儿肥大细胞介导依赖于母体 IgE 的产后过敏反应

母体 IgE 激活胎儿肥大细胞 肥大细胞 (MC) 是通过免疫球蛋白 E (IgE) 抗体的激活参与过敏反应的免疫细胞。MCs 在哺乳动物发育早期出现，但尚不清楚 IgE 介导的激活是否发生在胎儿组织中以及 IgE 刺激的来源是什么。姆萨拉姆等人。表明人和小鼠胎儿 MC 可以被母体来源的 IgE 致敏，其通过胎儿新生儿 Fc 受体穿过胎盘屏障（参见 Rothenberg 的观点）。产前母体致敏在出生后赋予短暂的过敏原敏感性，并导致后代在首次接触过敏原后出现出生后皮肤和气道炎症。因此，母体 IgE 和胎儿 MCs 都可能影响妊娠期间过敏性疾病的母婴传播。科学，这个问题 p。941; 另见第。907 母体衍生的免疫球蛋白 E 可使后代在接触过敏原后在新生儿和生命早期易患过敏性疾病。肥大细胞 (MC) 是过敏反应中的中枢效应细胞，通常由免疫球蛋白 E (IgE) 介导。过敏通常在很小的时候就开始了，并且在胎儿中都可以检测到 MCs 和 IgE。然而，胎儿 IgE 的起源以及胎儿 MC 是否可以响应 IgE 依赖性激活而脱颗粒，目前尚不清楚。在这里，我们表明人类和小鼠胎儿 MCs 表型在怀孕期间成熟，并且可以被母体 IgE 致敏。IgE 穿过胎盘，依赖于胎儿新生儿 Fc 受体 (FcRN)，并使胎儿 MC 对过敏原特异性脱颗粒敏感。被动和主动产前致敏都赋予了过敏原敏感性，在第一次接触过敏原后导致产后皮肤和气道炎症。我们报告了 MCs 在发育中的胎儿中的作用，并证明胎儿 MCs 可能有助于过敏性疾病的抗原特异性垂直传播。