The BCL6 RD2 Domain Governs Commitment of Activated B Cells to Form Germinal Centers Academic Article uri icon


MeSH Major

  • B-Lymphocytes
  • DNA-Binding Proteins
  • Germinal Center


  • To understand how the Bcl6 transcriptional repressor functions in the immune system, we disrupted its RD2 repression domain in mice. Bcl6RD2(MUT) mice exhibit a complete loss of germinal center (GC) formation but retain normal extrafollicular responses. Bcl6RD2(MUT) antigen-engaged B cells migrate to the interfollicular zone and interact with cognate T helper cells. However, these cells fail to complete early GC-commitment differentiation and coalesce as nascent GC aggregates. Bcl6 directly binds and represses trafficking receptors S1pr1 and Gpr183 by recruiting Hdac2 through the RD2 domain. Deregulation of these genes impairs B cell migration and may contribute to GC failure in Bcl6RD2(MUT) mice. The development of functional GC-TFH cells was partially impaired in Bcl6RD2(MUT) mice. In contrast to Bcl6(-/-) mice, Bcl6RD2(MUT) animals experience no inflammatory disease or macrophage deregulation. These results reveal an essential role for RD2 repression in early GC commitment and striking biochemical specificity in Bcl6 control of humoral and innate immune-cell phenotypes.

publication date

  • January 2014



  • Academic Article



  • eng

PubMed Central ID

  • PMC4163070

Digital Object Identifier (DOI)

  • 10.1016/j.celrep.2014.07.059

PubMed ID

  • 25176650

Additional Document Info

start page

  • 1497

end page

  • 508


  • 8


  • 5