Anti-T-bet / Tbox-bet / TBX21, clone TBX21/6724

1 mg/ml in 1X PBS, BSA free, sodium azide free. T helper (Th) lymphocytes differentiate into two unique subsets, Th1 and Th2, which differ both in function and in the cytokines they secrete. Th1 and Th2 cytokines promote the growth and differentiation of their subset, and inhibit the growth and differentiation of the opposing subset. T-bet (T-box expressed in T cells) is a Th1-specific T-box transcription factor that controls the expression of the Th1 cytokine, IFN-g. T-bet also converts effector Th2 cells into the opposing Th1 subset. T-bet is selectively expressed in Th1 cells. The level of T-bet expression is increased by signals mediated by the T cell receptor (TCR). IL-12 also induces an increase in the level of T-bet. T-bet was originally isolated from nuclear extracts of resting and PMA/ionomycin-activated AE7 cells. It is expressed in low levels in AE7 cells, and in increased levels in stimulated AE7. Protein function: Lineage-defining transcription factor which initiates Th1 lineage development from naive Th precursor cells both by activating Th1 genetic programs and by repressing the opposing Th2 and Th17 genetic programs (PubMed:10761931). Activates transcription of a set of genes important for Th1 cell function, including those encoding IFN- gamma and the chemokine receptor CXCR3. Induces permissive chromatin accessibilty and CpG methylation in IFNG (PubMed:33296702). Activates IFNG and CXCR3 genes in part by recruiting chromatin remodeling complexes including KDM6B, a SMARCA4-containing SWI/SNF-complex, and an H3K4me2-methyltransferase complex to their promoters and all of these complexes serve to establish a more permissive chromatin state conducive with transcriptional activation. Can activate Th1 genes also via recruitment of Mediator complex and P-TEFb (composed of CDK9 and CCNT1/cyclin-T1) in the form of the super elongation complex (SEC) to super-enhancers and associated genes in activated Th1 cells (PubMed:27292648). Inhibits the Th17 cell lineage commitment by blocking RUNX1-mediated transactivation of Th17 cell-specific transcriptinal regulator RORC. Inhibits the Th2 cell lineage commitment by suppressing the production of Th2 cytokines, such as IL-4, IL-5, and IL- 13, via repression of transcriptional regulators GATA3 and NFATC2. Protects Th1 cells from amplifying aberrant type-I IFN response in an IFN-gamma abundant microenvironment by acting as a repressor of type-I IFN transcription factors and type-I IFN-stimulated genes. Acts as a regulator of antiviral B-cell responses, controls chronic viral infection by promoting the antiviral antibody IgG2a isotype switching and via regulation of a broad antiviral gene expression program. Required for the correct development of natural killer (NK) and mucosal-associated invariant T (MAIT) cells (PubMed:33296702). [The UniProt Consortium]