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Promoter Confers Th1 Selective Expression1
* Division of Rheumatology, Departments of Medicine, and
Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232
Th1 and Th2 cells differentiate from naive precursors to effector
cells that produce either IFN-
or IL-4, respectively. To identify
transcriptional paths leading to activation and silencing of the
IFN- gene, we analyzed transgenic mice that express a reporter gene
under the control of the 5' IFN- promoter. We found that as the
length of the promoter is increased, -110 to -225 to -565 bp, the
activity of the promoter undergoes a transition from Th1 nonselective
to Th1 selective. This is due, at least in part, to a T box expressed
in T cells-responsive unit within the -565 to -410 region of the
IFN- promoter. The -225 promoter is silent when compared with the
-110 promoter and silencing correlates with Yin Yang 1 binding to the
promoter. The p38 mitogen-activated protein kinase signaling pathway,
which also regulates IFN- gene transcription, regulates the -70- to
-44-bp promoter element. Together, the results demonstrate that a
minimal IFN- promoter contains a T box expressed in T cells
responsive unit and is sufficient to confer Th1 selective expression
upon a reporter.
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