Journal
SCIENCE
Volume 325, Issue 5943, Pages 1001-1005Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1176676
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Funding
- NIH
- M. D. Anderson Cancer Center
- Leukemia and Lymphoma Society
- Schissler Foundation
- Korea Science and Engineering Foundation
- American Heart Association
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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 T(H)1, T(H)2, and T(H)17 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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