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* Howard Hughes Medical Institute, Departments of
Medicine and Microbiology/Immunology, and
Biochemistry and Biophysics, University of California, San Francisco, CA 94143; and
Genome Sciences Department, Lawrence Berkeley National Laboratory, Berkeley, CA 94720
Chromatin immunoprecipitations in naive CD4, but not CD8, T cells, demonstrated association of the IL-4 promoter with acetylated histone. Histone modifications and rapid IL-4 transcription were absent in conserved noncoding sequence 1 (CNS-1)-/- cells lacking an 8-kb-distant enhancer in the IL-4/IL-13 intergenic region, but also in CD4-/- and Itk-/- cells, which have similar Th2 deficiencies. Histones associated with the IL-13 promoter were not similarly acetylated in naive T cells, but became acetylated in differentiated Th2 cells. Conversely, Th1 differentiation induced histone methylation at the type 2 cytokine locus. Like CD4-/- and Itk-/- mice, CNS-1-/- BALB/c mice were highly resistant to the Th2-inducing protozoan, Leishmania major. CNS-1 deficiency led to failure of IL-4 gene repositioning to heterochromatin after Th1 polarization, possibly related to the presence of reiterative Ikaros binding sites in the intergenic element. Hyperacetylation of nonexpressed genes may serve to mark lineage-specific loci for rapid expression and further modification.
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