Postnatal regulation of B-1a cell development and survival by the CIC-PER2-BHLHE41 axis

Hyebeen Hong, Jongeun Lee, Guk Yeol Park, Soeun Kim, Jiho Park, Jong Seok Park, Youngkwon Song, Sujin Lee, Tae Jin Kim, You Jeong Lee, Tae Young Roh, Seung Ki Kwok, Sung Won Kim, Qiumin Tan, Yoontae Lee

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6 Scopus citations


B-1 cell development mainly occurs via fetal and neonatal hematopoiesis and is suppressed in adult bone marrow hematopoiesis. However, little is known about the factors inhibiting B-1 cell development at the adult stage. We report that capicua (CIC) suppresses postnatal B-1a cell development and survival. CIC levels are high in B-1a cells and gradually increase in transitional B-1a (TrB-1a) cells with age. B-cell-specific Cic-null mice exhibit expansion of the B-1a cell population and a gradual increase in TrB-1a cell frequency with age but attenuated B-2 cell development. CIC deficiency enhances B cell receptor (BCR) signaling in transitional B cells and B-1a cell viability. Mechanistically, CIC-deficiency-mediated Per2 derepression upregulates Bhlhe41 levels by inhibiting CRY-mediated transcriptional repression for Bhlhe41, consequently promoting B-1a cell formation in Cic-null mice. Taken together, CIC is a key transcription factor that limits the B-1a cell population at the adult stage and balances B-1 versus B-2 cell formation.

Original languageEnglish
Article number110386
JournalCell Reports
Issue number7
StatePublished - 15 Feb 2022

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  • B cell development
  • B-1a
  • BCR signaling
  • BHLHE41
  • PER2
  • TrB-1a
  • capicua


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