Mouse Hobit is a homolog of the transcriptional repressor Blimp-1 that regulates NKT cell effector differentiation

Klaas P. J. M. van Gisbergen, Natasja A. M. Kragten, Kirsten M. L. Hertoghs, Felix M. Wensveen, Stipan Jonjic, Jörg Hamann, Martijn A. Nolte, Rene A. W. van Lier

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Abstract

The transcriptional repressor Blimp-1 mediates the terminal differentiation of many cell types, including T cells. Here we identified Hobit (Znf683) as a previously unrecognized homolog of Blimp-1 that was specifically expressed in mouse natural killer T cells (NKT cells). Through studies of Hobit-deficient mice, we found that Hobit was essential for the formation of mature thymic NKT cells. In the periphery, Hobit repressed the accumulation of interferon-gamma (IFN-gamma)-producing NK1.1(lo) NKT cells at steady state. After antigenic stimulation, Hobit repressed IFN-gamma expression, whereas after innate stimulation, Hobit induced granzyme B expression. Thus, reminiscent of the function of Blimp-1 in other lymphocytes, Hobit controlled the maintenance of quiescent, fully differentiated NKT cells and regulated their immediate effector functions
Original languageEnglish
Pages (from-to)864-871
JournalNature immunology
Volume13
Issue number9
DOIs
Publication statusPublished - 2012

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