Journal
BLOOD
Volume 115, Issue 15, Pages 2989-2997Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2009-10-233585
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Funding
- FWF [SFB-021, P19505-B05]
- Tyrolian Science Fund [TWF-2008-1-563]
- Swiss Kamillo Eisner-Foundation [CH-6052]
- European Community [HEALTH-F4-2008-201106)]
- Austrian Federal Ministry of Science and Research [BMWF-651.423/0001-11/2/2009]
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The Ca2+ dependent transcription factor family known as nuclear factor of activated T cells (NFAT) has been shown to be important in T-cell immune responses. Because NFAT proteins have a weak DNA-binding capacity, they cooperate with other transcription factors at composite sites within the promoters of target genes. Recently, NFAT was shown to also be important for the induction of specific genetic programs that guide the differentiation and effector or regulatory activities of CD4(+) T helper subsets via the transcriptional regulation of their lineage-specific transcription factors, specifically T-bet (Th1), Gata3 (Th2), ROR gamma t (Th17), and Foxp3 (iTregs). In addition, the NFAT family governs the transcription of several signature cytokines, including their cytokine receptors. Subsequently, the integration of these complex intracellular signal transduction cascades is considered to critically determine the crosstalk between the T-cell receptor and receptors that are activated by both the adaptive and innate immune systems to determine pathways of T helper cell differentiation and function. Here, we carefully review the critical role of the established transcriptional partners and functional outcomes of these NFAT interactions in regard to the effector responses of these clinically relevant CD4(+) T helper subsets. (Blood. 2010; 115(15): 2989-2997)
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