Histone chaperone CHAF1B facilitates germinal center B cell differentiation via cooperation with BCL6 and TBL1XR1
Despite significant advances in the understanding on the regulation of BCL6 and its complexes in germinal center (GC), many aspects of this regulation remain unclear. For example, the broader implications of BCL6's interaction with other transcription factors and chromatin remodelers in GC dynamics require more detailed explorations. Here, through co-Immunoprecipitation coupled with mass spectrometry, we identify CHAF1B as a new partner in the BCL6 complex, promoting GC formation and immune responses. Mechanism, CHAF1B stabilizes BCL6/TBL1XR1 complex to promote GC B cell differentiation by cooperative transcriptional repression. Furthermore, overexpression of CHAF1B in B cells could reduce the plasmablast by extending GC reaction, which is positively related to the production of high affinity antibodies in response to vaccines or pathogens. These findings not only advance the understanding of GC biology but also had potential implications for developing targeted strategies to improve vaccination efficacy.