Abstract
Intestinal microfold cells (M cells) are an enigmatic lineage of intestinal epithelial cells that initiate mucosal immune responses through the uptake and transcytosis of luminal antigens. The mechanisms of M-cell differentiation are poorly understood, as the rarity of these cells has hampered analysis. Exogenous administration of the cytokine RANKL can synchronously activate M-cell differentiation in mice. Here we show the Ets transcription factor Spi-B was induced early during M-cell differentiation. Absence of Spi-B silenced the expression of various M-cell markers and prevented the differentiation of M cells in mice. The activation of T cells via an oral route was substantially impaired in the intestine of Spi-B-deficient (Spib -/-) mice. Our study demonstrates that commitment to the intestinal M-cell lineage requires Spi-B as a candidate master regulator.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 729-736 |
| Number of pages | 8 |
| Journal | Nature Immunology |
| Volume | 13 |
| Issue number | 8 |
| DOIs | |
| State | Published - Aug 2012 |
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ASJC Scopus subject areas
- Immunology
Cite this
The Ets transcription factor Spi-B is essential for the differentiation of intestinal microfold cells. / Kanaya, Takashi; Hase, Koji; Takahashi, Daisuke; Fukuda, Shinji; Hoshino, Katsuaki; Sasaki, Izumi; Hemmi, Hiroaki; Knoop, Kathryn A.; Kumar, Nachiket; Sato, Mayuko; Katsuno, Tatsuro; Yokosuka, Osamu; Toyooka, Kiminori; Nakai, Kumiko; Sakamoto, Ayako; Kitahara, Yuuki; Jinnohara, Toshi; Mcsorley, Stephen J; Kaisho, Tsuneyasu; Williams, Ifor R.; Ohno, Hiroshi.
In: Nature Immunology, Vol. 13, No. 8, 08.2012, p. 729-736.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The Ets transcription factor Spi-B is essential for the differentiation of intestinal microfold cells
AU - Kanaya, Takashi
AU - Hase, Koji
AU - Takahashi, Daisuke
AU - Fukuda, Shinji
AU - Hoshino, Katsuaki
AU - Sasaki, Izumi
AU - Hemmi, Hiroaki
AU - Knoop, Kathryn A.
AU - Kumar, Nachiket
AU - Sato, Mayuko
AU - Katsuno, Tatsuro
AU - Yokosuka, Osamu
AU - Toyooka, Kiminori
AU - Nakai, Kumiko
AU - Sakamoto, Ayako
AU - Kitahara, Yuuki
AU - Jinnohara, Toshi
AU - Mcsorley, Stephen J
AU - Kaisho, Tsuneyasu
AU - Williams, Ifor R.
AU - Ohno, Hiroshi
PY - 2012/8
Y1 - 2012/8
N2 - Intestinal microfold cells (M cells) are an enigmatic lineage of intestinal epithelial cells that initiate mucosal immune responses through the uptake and transcytosis of luminal antigens. The mechanisms of M-cell differentiation are poorly understood, as the rarity of these cells has hampered analysis. Exogenous administration of the cytokine RANKL can synchronously activate M-cell differentiation in mice. Here we show the Ets transcription factor Spi-B was induced early during M-cell differentiation. Absence of Spi-B silenced the expression of various M-cell markers and prevented the differentiation of M cells in mice. The activation of T cells via an oral route was substantially impaired in the intestine of Spi-B-deficient (Spib -/-) mice. Our study demonstrates that commitment to the intestinal M-cell lineage requires Spi-B as a candidate master regulator.
AB - Intestinal microfold cells (M cells) are an enigmatic lineage of intestinal epithelial cells that initiate mucosal immune responses through the uptake and transcytosis of luminal antigens. The mechanisms of M-cell differentiation are poorly understood, as the rarity of these cells has hampered analysis. Exogenous administration of the cytokine RANKL can synchronously activate M-cell differentiation in mice. Here we show the Ets transcription factor Spi-B was induced early during M-cell differentiation. Absence of Spi-B silenced the expression of various M-cell markers and prevented the differentiation of M cells in mice. The activation of T cells via an oral route was substantially impaired in the intestine of Spi-B-deficient (Spib -/-) mice. Our study demonstrates that commitment to the intestinal M-cell lineage requires Spi-B as a candidate master regulator.
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UR - http://www.scopus.com/inward/citedby.url?scp=84864147310&partnerID=8YFLogxK
U2 - 10.1038/ni.2352
DO - 10.1038/ni.2352
M3 - Article
VL - 13
SP - 729
EP - 736
JO - Nature Immunology
JF - Nature Immunology
SN - 1529-2908
IS - 8
ER -