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

研究成果: Article査読

15 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)250-255
ページ数6
ジャーナルAnnals of the New York Academy of Sciences
1362
1
DOI
出版ステータスPublished - 2015 12月 1

ASJC Scopus subject areas

  • 神経科学一般
  • 生化学、遺伝学、分子生物学一般
  • 科学史および科学哲学

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