Bcl6 Mediates the Development of T Follicular Helper Cells

Roza Nurieva(The University of Texas MD Anderson Cancer Center), Yeonseok Chung(The University of Texas MD Anderson Cancer Center), Gustavo Martínez(The University of Texas MD Anderson Cancer Center), Xuexian O. Yang(The University of Texas MD Anderson Cancer Center), Shinya Tanaka(The University of Texas MD Anderson Cancer Center), Tatyana D. Matskevitch(The University of Texas MD Anderson Cancer Center), Yi-Hong Wang(The University of Texas MD Anderson Cancer Center), Chen Dong(The University of Texas MD Anderson Cancer Center)
Science
July 24, 2009
10.1126/science.1176676
Cited by 1,477Open Access
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Abstract

A fundamental function of CD4+ helper T (T(H)) cells is the regulation of B cell-mediated humoral immunity. Development of T follicular helper (T(FH)) cells that provide help to B cells is mediated by the cytokines interleukin-6 and interleukin-21 but is independent of TH1, TH2, and TH17 effector cell lineages. Here, we characterize the function of Bcl6, a transcription factor selectively expressed in T(FH) cells. Bcl6 expression is regulated by interleukin-6 and interleukin-21. Bcl6 overexpression induced T(FH)-related gene expression and inhibited other T(H) lineage cell differentiation in a DNA binding-dependent manner. Moreover, Bcl6 deficiency in T cells resulted in impaired T(FH) cell development and germinal center reactions, and altered production of other effector T cell subsets. Our data thus illustrate that Bcl6 is required for programming of T(FH) cell generation.

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