IndraLab
Statements
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"Together, these data support the hypothesis that T-bet is required to inhibit the modest amounts of Bcl-6 expressed in effector T H 1 cells to prevent Bcl-6 from dominantly repressing the expression of glycolysis pathway genes and that this activity is functionally important for promoting glycolysis in effector T H 1 cells."
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"Strikingly, a bifurcation between Tfh and effector Th cells was measurable by the second cell division of CD4 + T cells, at day 2 after an acute viral infection : IL2Ralpha int cells expressed Bcl6 and CXCR5 (Tfh cell program), whereas IL2Ralpha hi cells exhibited strong Blimp1 expression that repressed Bcl6 (effector Th cell program)."
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"As a consequence of the mutations, CREBBP and EP300 lose their ability to acetylate BCL-6 and p53, a post-translational modification that inactivates BCL-6 by disrupting the recruitment of histone deacetylases (HDACs) and thus hindering its capacity to repress transcription, while representing an essential requirement for p53 activation XREF_BIBR - XREF_BIBR."