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Background  Id3 is a dominant antagonist of E protein transcription factor activity that is induced by signals emanating from the αβ and γδ T cell receptor (TCR). Mice lacking  Id3  were previously shown to have subtle defects in positive and negative selection of TCRαβ +  T lymphocytes. More recently,  Id3   −/−  mice on a C57BL/6 background were shown to have a dramatic expansion of γδ T cells.    Methodology/Principal Findings  Here we report that mice lacking Id3 have reduced thymocyte numbers but increased production of γδ T cells that express a Vγ1.1 + Vδ6.3 +  receptor with restricted junctional diversity. These Vγ1.1 + Vδ6.3 +  T cells have multiple characteristics associated with “innate” lymphocytes such as natural killer T (NKT) cells including an activated phenotype, expression of the transcription factor PLZF, and rapid production of IFNg and interleukin-4. Moreover, like other “innate” lymphocyte populations, development of  Id3   −/−  Vγ1.1 + Vδ6.3 +  T cells requires the signaling adapter protein SAP.    Conclusions  Our data provide novel insight into the requirements for development of Vγ1.1 + Vδ6.3 +  T cells and indicate a role for Id3 in repressing the response of “innate” γδ T cells to SAP-mediated expansion or survival.

Inhibitor of DNA Binding 3 Limits Development of Murine Slam-Associated Adaptor Protein-Dependent “Innate” γδ T cells