Perspectives on fetal derived CD5+ B1 B cells

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 IgMhighIgDlowCD5+, whereas adult cells IgMlowIgDhighCD5–. 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‐7 miRNA, 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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