TAO-kinase 3 governs the terminal differentiation of NOTCH2-dependent splenic conventional dendritic cells.

Proceedings of the National Academy of Sciences of the United States of America
Matthias VanderkerkenBart N Lambrecht

Abstract

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.

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Citations

Sep 17, 2021·Proceedings of the National Academy of Sciences of the United States of America·Nathalie DienerRonald A Backer
Sep 11, 2021·The Journal of Allergy and Clinical Immunology·Bastiaan MaesHamida Hammad
Oct 12, 2021·Molecular Metabolism·Ying XiaMargit Mahlapuu

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