CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation

CD69 competes with S1P1, a chemokine receptor mediating thymocyte egress, for surface expression on thymocytes, but whether CD69 is required for normal thymic development is unclear. Here the authors show that CD69 and S1P1 synergize to control type 2 natural killer (NKT2) cells differentiation by m...

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Autores principales:	Motoko Y. Kimura, Akemi Igi, Koji Hayashizaki, Yukiyoshi Mita, Miho Shinzawa, Tejas Kadakia, Yukihiro Endo, Satomi Ogawa, Ryoji Yagi, Shinichiro Motohashi, Alfred Singer, Toshinori Nakayama
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/610ec23ec8e14597aab0581e48fe6d35
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spelling	oai:doaj.org-article:610ec23ec8e14597aab0581e48fe6d352021-12-02T16:49:19ZCD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation10.1038/s41467-018-06283-12041-1723https://doaj.org/article/610ec23ec8e14597aab0581e48fe6d352018-09-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-06283-1https://doaj.org/toc/2041-1723CD69 competes with S1P1, a chemokine receptor mediating thymocyte egress, for surface expression on thymocytes, but whether CD69 is required for normal thymic development is unclear. Here the authors show that CD69 and S1P1 synergize to control type 2 natural killer (NKT2) cells differentiation by modulating the thymic egress of NKT2 precursor.Motoko Y. KimuraAkemi IgiKoji HayashizakiYukiyoshi MitaMiho ShinzawaTejas KadakiaYukihiro EndoSatomi OgawaRyoji YagiShinichiro MotohashiAlfred SingerToshinori NakayamaNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-12 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Motoko Y. Kimura Akemi Igi Koji Hayashizaki Yukiyoshi Mita Miho Shinzawa Tejas Kadakia Yukihiro Endo Satomi Ogawa Ryoji Yagi Shinichiro Motohashi Alfred Singer Toshinori Nakayama CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation
description	CD69 competes with S1P1, a chemokine receptor mediating thymocyte egress, for surface expression on thymocytes, but whether CD69 is required for normal thymic development is unclear. Here the authors show that CD69 and S1P1 synergize to control type 2 natural killer (NKT2) cells differentiation by modulating the thymic egress of NKT2 precursor.
format	article
author	Motoko Y. Kimura Akemi Igi Koji Hayashizaki Yukiyoshi Mita Miho Shinzawa Tejas Kadakia Yukihiro Endo Satomi Ogawa Ryoji Yagi Shinichiro Motohashi Alfred Singer Toshinori Nakayama
author_facet	Motoko Y. Kimura Akemi Igi Koji Hayashizaki Yukiyoshi Mita Miho Shinzawa Tejas Kadakia Yukihiro Endo Satomi Ogawa Ryoji Yagi Shinichiro Motohashi Alfred Singer Toshinori Nakayama
author_sort	Motoko Y. Kimura
title	CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation
title_short	CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation
title_full	CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation
title_fullStr	CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation
title_full_unstemmed	CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation
title_sort	cd69 prevents plzfhi innate precursors from prematurely exiting the thymus and aborting nkt2 cell differentiation
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/610ec23ec8e14597aab0581e48fe6d35
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CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation

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