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

doi:10.1111/nyas.12768

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

School of Pharmacy

Research output: Contribution to journal › Article › peer-review

15 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 language	English
Pages (from-to)	250-255
Number of pages	6
Journal	Annals of the New York Academy of Sciences
Volume	1362
Issue number	1
DOIs	https://doi.org/10.1111/nyas.12768
Publication status	Published - 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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10.1111/nyas.12768

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title = "B cells generated by B-1 development can progress to chronic lymphocytic leukemia",

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.",

keywords = "Autoreactive BCR, B cell subsets, B-1 development, B-CLL, B1a",

author = "Kyoko Hayakawa and Formica, {Anthony M.} and Colombo, {Matthew J.} and Daiju Ichikawa and Shinton, {Susan A.} and Joni Brill-Dashoff and Hardy, {Richard R.}",

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AU - Hayakawa, Kyoko

AU - Formica, Anthony M.

AU - Colombo, Matthew J.

AU - Ichikawa, Daiju

AU - Shinton, Susan A.

AU - Brill-Dashoff, Joni

AU - Hardy, Richard R.

PY - 2015/12/1

Y1 - 2015/12/1

N2 - 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.

AB - 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.

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KW - B cell subsets

KW - B-1 development

KW - B-CLL

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

Abstract

Keywords

ASJC Scopus subject areas

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