期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 111, 期 16, 页码 5986-5991出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1401671111
关键词
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资金
- Japan Society for the Promotion of Science
- Grants-in-Aid for Scientific Research [24111511] Funding Source: KAKEN
The gastrointestinal tract comes into direct contact with environmental agents, including bacteria, viruses, and foods. Intestine-specific subsets of immune cells maintain gut homeostasis by continuously sampling luminal antigens and maintaining immune tolerance. CD11c(+)CX(3)CR1(+) cells sample luminal antigens in the small intestine and contribute to the trafficking of bacteria to lymph nodes under dysbiotic conditions. The molecular mechanisms crucial for the differentiation of CD11c(+)CX(3)CR1(+) cells remain unclear. Here we demonstrate that the Notch1- or Notch2-Rbpj axis is essential for the development of CD11c(+)CX(3)CR1(+) cells. In mice in which Rbpj or Notch1 and Notch2 were deleted from CD11c(+) cells, there was a deficit of CD11c(+)CX(3)CR1(+) cells and an accumulation of CD11c(low)CX(3)CR1(+) cells. The CD11c(low)CX(3)CR1(+) cells could not differentiate to CD11c(+)CX(3)CR1(+) cells, suggesting that CD11c(low)CX(3)CR1(+) cells represent a lineage distinct from CD11c(+)CX(3)CR1(+) cells. These data indicate that Notch signaling is essential for lineage fixation of intestinal CD11c(+)CX(3)CR1(+) cells.
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