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10.4049/jimmunol.1500200

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C4456636!4456636!25957170
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suck abstract from ncbi


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pmid25957170      J+Immunol 2015 ; 194 (12): 5599-603
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  • Cutting Edge: T Follicular Helper Cell Differentiation Is Defective in the Absence of Bcl6 BTB Repressor Domain Function #MMPMID25957170
  • Nance JP; Bélanger S; Johnston RJ; Takemori T; Crotty S
  • J Immunol 2015[Jun]; 194 (12): 5599-603 PMID25957170show ga
  • T follicular helper (Tfh) cells are essential for germinal centers (GCs) and most long-term humoral immunity. Differentiation of Tfh cells depends on the transcriptional repressor B cell CLL/lymphoma 6 (Bcl6). Bcl6 mediates gene repression via the recruitment of corepressors. Currently, it is unknown how Bcl6 recruits corepressors to regulate gene expression of Tfh cells. In this article, we demonstrate, using a mutant form of Bcl6 with two BTB (bric-a-brac, tramtrack, broad-complex) mutations that abrogate corepressor binding, that the Bcl6 BTB domain is required for proper differentiation of Tfh and GC-Tfh cells in vivo. Importantly, we also observe a significant defect in GC B cell development. These results are consistent in multiple contexts, including a novel lymphocytic choriomeningitis virus nucleoprotein-specific TCR-transgenic mouse model. Taken together, these data suggest that the Bcl6 BTB domain is a key mediator of the differentiation of Tfh cells.
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