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by 
T Cells1
Sections of
*
Rheumatology and
Pulmonary and Critical Care Medicine, Department of Medicine, and
Section of Immunobiology, Yale School of Medicine, New Haven, CT 06520; and
Harvard School of Public Health, Boston, MA 02115
T cells predominantly produce IFN- upon activation. To
determine the basis for default production of IFN- by T
cells, we analyzed the transcription factors T-box expressed in T cells
(T-bet) and GATA-3. T-bet, absent in naive cells, was induced
upon TCR signaling, with IFN- production. T-bet also regulated IL-4
synthesis, as cells isolated from T-bet-deficient mice displayed
enhanced IL-4 levels with reduced IFN- production. Notably, T-bet
expression after TCR signaling in cells was not down-regulated
by IL-4, in conjunction with a higher ratio of T-bet:GATA-3 expression
than that found in CD4+ T cells. Indeed, overexpression of
GATA-3 failed to inhibit IFN- secretion in cells to the
degree seen in CD4+ T cells. These results indicate that
T-bet enhances IFN- secretion and suppresses IL-4 secretion
in cells, and that GATA-3 fails to counterbalance T-bet-mediated
IFN- production, accounting for the default synthesis of IFN- by
these T lymphocytes.
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