Acquisition of transcriptional competence during differentiation of T helper cells. Th cells become productive effectors of immunoinflammatory responses following a complex series of molecular events dependent upon membrane-proximal TCRs and cytokine receptor signals. Chromatin remodelling is an essential step in the process leading to a switch from the 'closed' to 'open' DNA conformation. This in turn permits accessibility of Th-subset-specific transcription factors and accessory factors to the promoter elements of the Th2 gene cluster, as illustrated here. Ultimately, NFAT is recruited to the transcriptosome, after which cytokine gene transcription proceeds. c-Maf, transcription factor specific for Th2 cells; ERM, transcription factor specific for Th1 cells; GATA-3, transcription factor specific for Th2 cells; NFAT, nuclear factor of activated T cells; STAT, signal transducer and activator of transcription; T-bet, transcription factor specific for Th1 cells; TCR, T-cell receptor; Th, T helper (cell).