Transgenic major histocompatibility complex class I antigen expressed in mouse trophoblast affects maternal immature B cells
Transgenic major histocompatibility complex class I antigen expressed in mouse trophoblast affects maternal immature B cells
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DOI：
10.1095/biolreprod65.2.337
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发表时间：
2001-08-01
影响因子：
3.6
通讯作者：
Kanellopoulos-Langevin, C
中科院分区：
文献类型：
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作者：
Aït-Azzouzene, D;Caucheteux, S;Kanellopoulos-Langevin, C
我们已经产生了转基因小鼠，使用小鼠胎盘催乳素II型启动子，迫使和限制表达的小鼠主要组织相容性复合体（MHC）I类分子，H-2 K（B），胎盘。我们发现，转基因MHC抗原H-2K（B）只表达在滋养层巨细胞从第10.5天，直到妊娠结束。这种表达既不影响胎儿发育，也不影响组织不相容母体对胎儿的耐受性。我们使用3.83 B细胞受体（BcR）转基因小鼠系来跟踪携带H-2K（B）阳性胎盘的母亲中H-2K（B）特异性母体B细胞的命运。我们的研究结果表明，滋养层巨细胞上的转基因H-2K（B）分子被妊娠女性骨髓中的3.83 BcR转基因B细胞识别。这种抗原识别触发骨髓IS细胞亚群的缺失，包括未成熟和过渡性B细胞。其百分比在妊娠后半期降低，第17.5天降至8%，而（3.83 Tg雌性x Fvb）对照组为22%。这种缺失可能有助于母体对孕体的耐受过程。
We have produced transgenic mice using the mouse placental lactogen type II promoter to force and restrict the expression of the mouse major histocompatibility complex (MHC) class I molecule, H-2K(b), to the placenta. We show that the transgenic MHC antigen H-2K(b) is expressed exclusively in trophoblast giant cells from Day 10.5 until the end of gestation. This expression affects neither the fetal development nor the maternal tolerance to the fetus in histoincompatible mothers. We have used the 3.83 B cell receptor (BcR) transgenic mouse line to follow the fate of H-2K(b)-Specific maternal B cells in mothers bearing H-2K(b)-positive placentas. Our results suggest that transgenic H-2K(b) molecules on trophoblast giant cells are recognized by 3.83 BcR-transgenic B cells in the bone marrow of pregnant females. This antigen recognition triggers the deletion of a bone marrow IS cell subpopulation, including immature and transitional B cells. Their percentage decreases during the second half of gestation and is down to 8% on Day 17.5, compared to 22% in the (3.83 Tg female x Fvb) control group. This deletion might contribute to the process of maternal tolerance of the conceptus.