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

Motoko Y. Kimura (), Akemi Igi, Koji Hayashizaki, Yukiyoshi Mita, Miho Shinzawa, Tejas Kadakia, Yukihiro Endo, Satomi Ogawa, Ryoji Yagi, Shinichiro Motohashi, Alfred Singer and Toshinori Nakayama
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Motoko Y. Kimura: Chiba University
Akemi Igi: Chiba University
Koji Hayashizaki: Chiba University
Yukiyoshi Mita: Chiba University
Miho Shinzawa: National Institutes of Health
Tejas Kadakia: National Institutes of Health
Yukihiro Endo: Chiba University
Satomi Ogawa: Chiba University
Ryoji Yagi: Chiba University
Shinichiro Motohashi: Chiba University
Alfred Singer: National Institutes of Health
Toshinori Nakayama: Chiba University

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract While CD69 may regulate thymocyte egress by inhibiting S1P1 expression, CD69 expression is not thought to be required for normal thymocyte development. Here we show that CD69 is in fact specifically required for the differentiation of mature NKT2 cells, which do not themselves express CD69. Mechanistically, CD69 expression is required on CD24+ PLZFhi innate precursors for their retention in the thymus and completion of their differentiation into mature NKT2 cells. By contrast, CD69-deficient CD24+ PLZFhi innate precursors express S1P1 and prematurely exit the thymus, while S1P1 inhibitor treatment of CD69-deficient mice retains CD24+ PLZFhi innate precursors in the thymus and restores NKT2 cell differentiation. Thus, CD69 prevents S1P1 expression on CD24+ PLZFhi innate precursor cells from aborting NKT2 differentiation in the thymus. This study reveals the importance of CD69 to prolong the thymic residency time of developing immature precursors for proper differentiation of a T cell subset.

Date: 2018
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DOI: 10.1038/s41467-018-06283-1

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