期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 45, 期 11, 页码 2978-2984出版社
WILEY
DOI: 10.1002/eji.201445146
关键词
B1a cells; B-cell development; B-cell leukemia; CD5(+) B cells; Stem cells; Transgenic mouse models
类别
资金
- NIH [RO1 AI026782, RC1 CA145445, RO1 CA129330, R01 AI049335]
- FCCC Blood Cell Development and Cancer Keystone initiative
CD5(+) B-cell origins and their predisposition to lymphoma are long-standing issues. Transfer of fetal and adult liver BM Pro-B cells generates B cells with distinct phenotypes: fetal cells generate IgM(high)IgD(low)CD5(+), whereas adult cells IgM(low)IgD(high)CD5(-). This suggests a developmental switch in B lymphopoiesis, similar to the switch in erythropoiesis. Comparison of mRNA and miRNA expression in fetal and adult Pro-B cells revealed differential expression of Lin28b mRNA and Let-7miRNA, providing evidence that this regulatory axis functions in the switch. Recent work has shown that Arid3a is a key transcription factor mediating fetal-type B-cell development. Lin28b-promoted fetal development generates CD5(+) B cells as a consequence of positively selected self-reactivity. CD5(+) B cells play important roles in clearance of apoptotic cells and in protective immune responses, but also pose a risk of progression to leukemia/lymphoma. Differential Lin28b expression in fetal and adult human B-cell precursors showed that human B-cell development may resemble mouse, with self-reactive innate-like B cells generated early in life. It remains to be determined whether such human B cells have a higher propensity to leukemic progression. This review describes our recent research with CD5(+) B cells and presents our perspective on their role in disease.
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