Abstract
When B cells respond to an infection, they often require help from CD4+ T cells to mount a proper response. It is thought that a subset of CD4+ effector T cells, called T follicular helper cells (TFH), performs this function. Several subsets of effector CD4+ T cells arise, depending on the type of infection, which have distinct transcriptional programs driving their differentiation. Whether this is also the case for TFH cells has not been clear (see the Perspective by [Awasthi and Kuchroo][1] ). Nurieva et al. (p. [1001][2], published online 23 July) and Johnston et al. (p. [1006][3]; published online 16 July) now demonstrate that the transcription factor Bcl6 is both necessary and sufficient for TFH differentiation and subsequent B cell–mediated immunity, suggesting that it is a master regulator of this lineage. Johnston et al. also show that expression of Bcl6 and the transcription factor, Blimp-1, are reciprocally regulated in TFH cells and that, when ectopically expressed, Blimp-1 inhibits TFH development. [1]: /lookup/doi/10.1126/science.1178752 [2]: /lookup/doi/10.1126/science.1176676 [3]: /lookup/doi/10.1126/science.1175870
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