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CUTTING EDGE |
*
Department of Medicine and
Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, Chicago, IL 60637; and
Laboratory of Cardiovascular Biology, Harvard School of Public Health and Harvard Medical School, Boston MA 02115
Ets1-deficient mice develop B and T cells but display a severe
defect in the development of the NK cell lineage. In this report, we
demonstrate that Ets1 is also required for the development of
NK1.1+ T (NK T) cells. We observed significantly decreased
numbers of NK T cells in the thymus, spleen, and liver of
Ets1-deficient mice. These organs also contained markedly decreased
levels of the canonical V
14-J281 TCR
transcript seen in NK T cells. Unlike wild-type NK T cells,
Ets1-deficient thymocytes failed to produce detectable levels of IL-4
following anti-CD3 stimulation. The absence of NK T cells in the
Ets1-deficient mice was not associated with defective expression of
CD1, an MHC class I molecule required for NK T cell development. We
conclude that Ets1 defines a novel transcriptional regulatory pathway
that is required for the development of both the NK and NK T cell
lineages.
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