Basal chromatin modification at the IL-4 gene in helper T cells
Journal Article
·
· Journal of Immunology
- LBNL Library
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){sup -/-} cells lacking an 8-kb-distant enhancer in the IL-4/IL-13 intergenic region, but also in CD4{sup -/-} and Itk{sup -/-} 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{sup -/-} and Itk{sup -/-} mice, CNS-1{sup -/-} 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.
- Research Organization:
- Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, CA (US)
- Sponsoring Organization:
- USDOE Director. Office of Science. Office of Biological and Environmental Research; National Institutes of Health Grants AI30663 and HL56385 and GM25101; Ellison Medical Foundation (US)
- DOE Contract Number:
- AC03-76SF00098
- OSTI ID:
- 834234
- Report Number(s):
- LBNL--55328
- Journal Information:
- Journal of Immunology, Journal Name: Journal of Immunology Journal Issue: 12 Vol. 171; ISSN 0022-1767; ISSN JOIMA3
- Country of Publication:
- United States
- Language:
- English
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