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lüll Molecular mechanisms by which T-bet regulates T-helper cell commitment Miller SA; Weinmann ASImmunol Rev 2010[Nov]; 238 (1): 233-46Current research suggests that a number of newly identified T-helper cell subsets retain a degree of context-dependent plasticity in their signature cytokine expression patterns. To understand this process, a major challenge is to determine the molecular mechanisms by which lineage-defining transcription factors regulate gene expression profiles in T-helper cells. This mechanistic information will aid in our interpretation of whether a T-helper cell state that expresses or retains the capacity to re-express a combination of lineage-defining transcription factors will have a stable or more flexible gene expression profile. Studies examining the developmental T-box transcription factor T-bet demonstrate the powerful information that is gained from combining in vivo analysis with basic biochemical and molecular mechanism approaches. Significantly, T-bet's ability to physically recruit epigenetic modifying complexes, in particular a Jmjd3 H3K27-demethylase and a Set7/9 H3K4-methyltransferase complex, to its target genes allows T-bet to effectively reverse and establish new epigenetic states. This observation suggests that until T-bet is permanently extinguished, T-helper cells will retain some plasticity toward a T-helper 1-like program. Therefore, insight into the complexity of T-helper cell commitment decisions will be aided by determining the molecular mechanisms for lineage-defining transcription factors.|Animals[MESH]|Cell Differentiation/*immunology[MESH]|Cell Lineage[MESH]|Epigenesis, Genetic/immunology[MESH]|Gene Expression Regulation, Developmental/immunology[MESH]|Histone Demethylases/*immunology[MESH]|Histone-Lysine N-Methyltransferase/*immunology[MESH]|Humans[MESH]|T-Box Domain Proteins/*immunology[MESH]|Th1 Cells/*immunology[MESH] |