First Author | Ishifune C | Year | 2014 |
Journal | Proc Natl Acad Sci U S A | Volume | 111 |
Issue | 16 | Pages | 5986-91 |
PubMed ID | 24711412 | Mgi Jnum | J:208857 |
Mgi Id | MGI:5565119 | Doi | 10.1073/pnas.1401671111 |
Citation | Ishifune C, et al. (2014) Differentiation of CD11c+CX3CR1+ cells in the small intestine requires Notch signaling. Proc Natl Acad Sci U S A 111(16):5986-91 |
abstractText | 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(+)CX3CR1(+) 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(+)CX3CR1(+) cells remain unclear. Here we demonstrate that the Notch1- or Notch2-Rbpj axis is essential for the development of CD11c(+)CX3CR1(+) cells. In mice in which Rbpj or Notch1 and Notch2 were deleted from CD11c(+) cells, there was a deficit of CD11c(+)CX3CR1(+) cells and an accumulation of CD11c(low)CX3CR1(+) cells. The CD11c(low)CX3CR1(+) cells could not differentiate to CD11c(+)CX3CR1(+) cells, suggesting that CD11c(low)CX3CR1(+) cells represent a lineage distinct from CD11c(+)CX3CR1(+) cells. These data indicate that Notch signaling is essential for lineage fixation of intestinal CD11c(+)CX3CR1(+) cells. |