Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, Sichuan, 611130, PR China.
Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, Sichuan, 611130, PR China.
Mol Immunol. 2018 Sep;101:120-129. doi: 10.1016/j.molimm.2018.06.266. Epub 2018 Jun 20.
As a central immune organ unique to birds, the bursa of Fabricius (BF) provides a proper microenvironment for B-cell development. The bursal B-cells undergo rapid proliferation and differentiation at the embryonic stages, but 95% of them undergo apoptosis after hatching. Few studies have focused on the cause of bursal B-cells apoptosis at the embryonic stages in birds. To explore the cause, we compared the transcriptional profiles of three characteristic embryonic stages in duck, including embryonic day 14 (ED14), 22 (ED22) and 1 day after hatching (D1). Our results showed that the apoptotic B-cells were first observed at ED22 while there were no apoptotic B-cells at ED14. By performing enrichment analysis for DEGs and qRT-PCR, our results demonstrated that both mitochondrial and Fas signaling pathways mediated bursal B-cell apoptosis during the duck embryonic development. Further, protein-protein interactions (PPIs) and KEGG enrichment analysis together showed that BMP4, FoxO1 and IGF-1 may regulate bursal B-cells apoptosis. In addition, the DEGs showed two stage-specific expression patterns. By analyzing the genes of two expression patterns, the results indicated that B-cell false differentiation may be one of the reasons of apoptosis in the duck embryonic BF. Overall, these data demonstrated that from ED14-ED22, apoptosis of bursal B-cells was mediated by mitochondrial and Fas signaling pathways and could be regulated by BMP4, FoxO1 and IGF-1 in duck. One of the primary causes of bursal B-cell apoptosis may be false differentiation in B-cells.
法氏囊作为鸟类特有的中枢免疫器官,为 B 细胞的发育提供了适宜的微环境。胚胎期的囊 B 细胞迅速增殖和分化,但 95%在孵化后凋亡。很少有研究关注鸟类胚胎期法氏囊 B 细胞凋亡的原因。为了探讨其原因,我们比较了鸭三个特征性胚胎期(ED14、ED22 和孵化后 1 天[D1])的转录谱。结果显示,凋亡的 B 细胞首先在 ED22 观察到,而 ED14 则没有凋亡的 B 细胞。通过对差异表达基因(DEGs)进行富集分析和 qRT-PCR,结果表明,线粒体和 Fas 信号通路都介导了鸭胚胎发育过程中法氏囊 B 细胞的凋亡。此外,蛋白质-蛋白质相互作用(PPIs)和 KEGG 富集分析共同表明,BMP4、FoxO1 和 IGF-1 可能调节法氏囊 B 细胞凋亡。此外,DEGs 显示出两种阶段特异性表达模式。通过分析两种表达模式的基因,结果表明 B 细胞假性分化可能是鸭胚胎 BF 中凋亡的原因之一。总之,这些数据表明,从 ED14 到 ED22,法氏囊 B 细胞的凋亡是由线粒体和 Fas 信号通路介导的,可以通过 BMP4、FoxO1 和 IGF-1 在鸭中进行调节。法氏囊 B 细胞凋亡的一个主要原因可能是 B 细胞的假性分化。