| First Author | Vanderkerken M | Year | 2020 |
| Journal | Proc Natl Acad Sci U S A | Volume | 117 |
| Issue | 49 | Pages | 31331-31342 |
| PubMed ID | 33214146 | Mgi Jnum | J:298569 |
| Mgi Id | MGI:6479931 | Doi | 10.1073/pnas.2009847117 |
| Citation | Vanderkerken M, et al. (2020) TAO-kinase 3 governs the terminal differentiation of NOTCH2-dependent splenic conventional dendritic cells. Proc Natl Acad Sci U S A 117(49):31331-31342 |
| abstractText | Antigen-presenting conventional dendritic cells (cDCs) are broadly divided into type 1 and type 2 subsets that further adapt their phenotype and function to perform specialized tasks in the immune system. The precise signals controlling tissue-specific adaptation and differentiation of cDCs are currently poorly understood. We found that mice deficient in the Ste20 kinase Thousand and One Kinase 3 (TAOK3) lacked terminally differentiated ESAM(+) CD4(+) cDC2s in the spleen and failed to prime CD4(+) T cells in response to allogeneic red-blood-cell transfusion. These NOTCH2- and ADAM10-dependent cDC2s were absent selectively in the spleen, but not in the intestine of Taok3 (-/-) and CD11c-cre Taok3 (fl/fl) mice. The loss of splenic ESAM(+) cDC2s was cell-intrinsic and could be rescued by conditional overexpression of the constitutively active NOTCH intracellular domain in CD11c-expressing cells. Therefore, TAOK3 controls the terminal differentiation of NOTCH2-dependent splenic cDC2s. |
