B cells generated by B-1 development can progress to chronic lymphocytic leukemia

Kyoko Hayakawa, Anthony M. Formica, Matthew J. Colombo, Daiju Ichikawa, Susan A. Shinton, Joni Brill-Dashoff, Richard R. Hardy

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)

Abstract

B cells generated early during fetal/neonatal B-1 development in mice include autoreactive cells with detectable CD5 upregulation induced by B cell receptor (BCR) signaling (B1a cells). A fraction of B1a cells are maintained by self-renewal for life, with the potential risk of dysregulated growth and progression to chronic lymphocytic leukemia (CLL)/lymphoma during aging. In studies using the Eμ-hTCL1 transgenic mouse system, it became clear that this B1a subset has a higher potential than other B cell subsets for progression to CLL. We have generated several autoreactive germline BCR gene models to compare B cells generated under conditions of natural exposure to autoantigen. Analysis of the mice has been key in understanding the importance of the BCR and BCR signaling for generating different B cell subsets and for investigating the cellular origin of B-CLL.

Original languageEnglish
Pages (from-to)250-255
Number of pages6
JournalAnnals of the New York Academy of Sciences
Volume1362
Issue number1
DOIs
Publication statusPublished - 2015 Dec 1

Keywords

  • Autoreactive BCR
  • B cell subsets
  • B-1 development
  • B-CLL
  • B1a

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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