CD69 prevents PLZF^hi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation.

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⁺ PLZF^hi innate precursors for their retention in the thymus and completion of their differentiation into mature NKT2 cells. By contrast, CD69-deficient CD24⁺ PLZF^hi innate precursors express S1P₁ and prematurely exit the thymus, while S1P₁ inhibitor treatment of CD69-deficient mice retains CD24⁺ PLZF^hi innate precursors in the thymus and restores NKT2 ce

SUBMITTER: Kimura MY 

PROVIDER: S-EPMC6138739 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature