The transfer of maternal antigen-specific IgG regulates the development of allergic airway inflammation early in life in an FcRn-dependent manner.
The transfer of maternal antigen-specific IgG regulates the development of allergic airway inflammation early in life in an FcRn-dependent manner.
复制标题
母体抗原特异性 IgG 的转移以 FcRn 依赖性方式调节生命早期过敏性气道炎症的发展。
DOI：
10.1016/j.bbrc.2010.03.170
复制
发表时间：
2010
影响因子：
3.1
通讯作者：
Nishimura,Yoshihiro
中科院分区：
文献类型：
--
作者：
Nakata,Kyosuke;Kobayashi,Kazuyuki;Ishikawa,Yumiko;Yamamoto,Masatsugu;Funada,Yasuhiro;Kotani,Yoshikazu;Blumberg,RichardS;Karasuyama,Hajime;Yoshida,Masaru;Nishimura,Yoshihiro
哮喘是一种慢性炎症性气道疾病，其特征是气道高反应性、粘液产生增加和可逆性气道收缩。哮喘是一种复杂的遗传性状，是由环境因素引起的。母体抗原特异性IgG通过羊水、胎盘和母乳运输在被动免疫中起重要作用。首先，为了研究母体通过FcRn转运抗原特异性IgG的被动免疫是否调节变应性气道炎症，将卵清蛋白免疫的FcRn+/ -雌性小鼠与FcRn - / -雄性小鼠杂交，以评估卵清蛋白诱导的FcRn - / -后代的过敏性气道炎症程度。母体被动免疫以fcrn依赖的方式调节变应性气道炎症。其次，为了检验母体抗原特异性IgG1注射到母体中的作用，我们在野生型或FcRn+/−小鼠分娩后立即静脉注射卵清蛋白特异性IgG1。后代被致敏并被卵清蛋白激发。给泌乳小鼠抗原特异性IgG1以fcrn依赖的方式减少其后代的过敏性气道炎症。最后，为了排除除卵清蛋白特异性IgG1外的母体被动免疫因素，我们在出生后给子代口服卵清蛋白特异性IgG1。在哺乳期给子代口服卵清蛋白特异性IgG1以fcrn依赖的方式阻止过敏性气道炎症的发展。这些数据表明，母体抗原特异性IgG的转移在生命早期以fcrn依赖的方式调节变应性气道炎症的发展。
Asthma is a chronic inflammatory airway disease characterized by airway hyperreactivity, increased mucus production, and reversible airway contraction. Asthma is a complex genetic trait caused by environmental factors in genetically predisposed individuals. The transportation of maternal antigen-specific IgG via amniotic fluid, placenta and breast milk plays an important role in passive immunity. First, to examine whether maternal passive immunity by the transportation of antigen-specific IgG via FcRn regulates allergic airway inflammation, ovalbumin-immunized FcRn+/−female mice were bred with FcRn−/−male mice to evaluate the degree of ovalbumin-induced allergic airway inflammation of FcRn−/−offspring. Maternal passive immunity regulated allergic airway inflammation in an FcRn-dependent manner. Second, to examine the role of maternal antigen-specific IgG1 injection into mothers, we intravenously injected ovalbumin-specific IgG1 into wild-type or FcRn+/−mice immediately after they gave birth. The offspring were sensitized and challenged with ovalbumin. Antigen-specific IgG1 administered to lactating mice reduced allergic airway inflammation in their offspring in an FcRn-dependent manner. Last, to exclude the factor of maternal passive immunity other than ovalbumin-specific IgG1, we administered ovalbumin-specific IgG1 orally to offspring after birth. Oral administration of ovalbumin-specific IgG1 to offspring during the lactating period prevented the development of allergic airway inflammation in an FcRn-dependent manner. These data show that the transfer of maternal antigen-specific IgG regulates the development of allergic airway inflammation early in life in an FcRn-dependent manner.