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Cutting Edge |
in Th1/Tc1 Effector Cells1
* Division of Rheumatology, Department of Medicine, and
Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232
Using a transgenic approach, we analyzed the contribution of
introns located within the IFN-
gene and distal
regulatory regions to IFN- gene expression. Intron 1 and
3 from the IFN- gene displayed strong enhancer activity.
This activity appeared to be dependent upon integration into the genome
but resulted in a loss of Th1 selectivity. We also found that distal
regulatory elements are not required for high level expression of the
human IFN- gene, but rather for cell lineage-specific
expression. An 8.6-kb human IFN- transgene was
sufficient to yield high level expression but a 191-kb
IFN- transgene with 
90 kb of flanking 5' and 3'
sequence was necessary to achieve both high level and Th1 selective
expression of human IFN-.
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