期刊
IMMUNITY
卷 32, 期 6, 页码 852-862出版社
CELL PRESS
DOI: 10.1016/j.immuni.2010.06.011
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资金
- Academy of Finland [77773, 203725, 207490, 116639, 115939, 123864, 126063, 127575, 120569]
- European Commission [EC-FP7-SYBILLA-201106, EC-FP7-NANOMMUNE-214281, EC-FP7-DIABIMMUNE-202063]
- CIMO/Sitra
- Sigrid Juselius Foundation
- Department of Biotechnology, Government of India
- Turku University Hospital
- Academy of Finland (AKA) [115939, 123864, 116639, 207490, 126063, 203725, 77773, 115939, 207490, 126063, 203725, 116639, 123864, 77773] Funding Source: Academy of Finland (AKA)
Dissecting the molecular mechanisms by which T helper (Th) cells differentiate to effector Th2 cells is important for understanding the pathogenesis of immune-mediated diseases, such as asthma and allergy. Because the STAT6 transcription factor is an upstream mediator required for interleukin-4 (IL-4)-induced Th2 cell differentiation, its targets include genes important for this process. Using primary human CD4(+) T cells, and by blocking STAT6 with RNAi, we identified a number of direct and indirect targets of STAT6 with ChIP sequencing. The integration of these data sets with detailed kinetics of IL-4-driven transcriptional changes showed that STAT6 was predominantly needed for the activation of transcription leading to the Th2 cell phenotype. This integrated genome-wide data on IL-4- and STAT6-mediated transcription provide a unique resource for studies on Th cell differentiation and, in particular, for designing interventions of human Th2 cell responses.
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