Transcription factor Spi-B-dependent and -independent pathways for the development of Peyer's patch M cells

Transcription factor Spi-B-dependent and -independent pathways for the development of Peyer's patch M cells
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DOI:
10.1038/mi.2012.122
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发表时间:
2013-07-01
期刊:
影响因子:
8
通讯作者:
Kiyono, H.
Kiyono, H.
中科院分区:
医学1区
文献类型:
--
作者:
Sato, S.;Kaneto, S.;Kiyono, H.

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尽管微折叠细胞(M细胞)的许多生物学特征已经被了解多年,但M细胞发育和抗原识别的分子机制仍然不清楚。在这里,我们报告Umod是一种新型M细胞特异性基因,其翻译产物可能有助于M细胞的摄取功能。转录因子Spi-B也在非造血谱系的M细胞中特异性表达。Spi-B缺陷小鼠表现出大部分但不是全部的其他M细胞特异性基因和M细胞表面标志物的表达降低。而通过M细胞的鼠伤寒沙门氏菌的摄取在Spi-B缺陷型小鼠中明显减少,野生型和Spi-B缺陷型小鼠之间的组织内共生细菌的丰度相当。这些数据表明,有一个小的M-细胞群体的发育调控是Spi-B独立的,然而,Spi-B可能是一个候选的主调节M-细胞功能成熟和发育的另一种途径。
Although many of the biological features of microfold cells (M cells) have been known for many years, the molecular mechanisms of M-cell development and antigen recognition have remained unclear. Here, we report that Umod is a novel M-cell-specific gene, the translation products of which might contribute to the uptake function of M cells. Transcription factor Spi-B was also specifically expressed in M cells among non-hematopoietic lineages. Spi-B-deficient mice showed reduced expression of most, but not all, other M-cell-specific genes and M-cell surface markers. Whereas uptake of Salmonella Typhimurium via M cells was obviously reduced in Spi-B-deficient mice, the abundance of intratissue cohabiting bacteria was comparable between wild-type and Spi-B-deficient mice. These data indicate that there is a small M-cell population with developmental regulation that is Spi-B independent; however, Spi-B is probably a candidate master regulator of M-cell functional maturation and development by another pathway.