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

Author

Listed:
  • Motoko Y. Kimura

    (Chiba University
    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)

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.

Suggested Citation

  • 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, 2018. "CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation," Nature Communications, Nature, vol. 9(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06283-1
    DOI: 10.1038/s41467-018-06283-1
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