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Originally published online as doi:10.1189/jlb.0706457 on August 25, 2008

Published online before print August 25, 2008
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(Journal of Leukocyte Biology. 2008;84:1557-1564.)
© 2008 by Society for Leukocyte Biology

Characterization of phenotypically distinct B-cell subsets and receptor-stimulated mitogen-activated protein kinase activation in human cord blood B cells

Yun Jung Ha*, Yeung-Chul Mun{dagger}, Chu-Myong Seong{dagger} and Jong Ran Lee*,{ddagger},1

* Division of Life and Pharmaceutical Sciences and Center for Cell Signaling and Drug Discovery Research, Ewha Womans University, Seoul, Korea;
{dagger} Department of Hematology-Oncology, College of Medicine, Ewha Womans University, Seoul, Korea; and
{ddagger} Department of Life Science, College of Natural Sciences, Ewha Womans University, Seoul, Korea

1 Correspondence: Division of Life Science, College of Natural Sciences, Ewha Womans University, 11-1 Daehyun-Dong, Seodaemun-Gu, Seoul 120-750, Korea. E-mail: jrlee{at}ewha.ac.kr

Human cord blood (CB) is a valuable source of hematopoietic stem cells, but clinical reports have indicated slow recovery of B-cell development and function after CB transplantation. To investigate the basis of these B-cell defects in reconstitution, we characterized B cells purified from CB. We compared B-cell receptor activation and B-cell subsets in CB, bone marrow (BM), and peripheral blood (PB). We found that in CB B cells activation of extracellular signal-regulated kinase (ERK) and p38 following ligation of CD40 but not of the B-cell antigen receptor (BCR) was inefficient. The patterns of expression of CD5, CD34, and CD40 in the B-cell population of CB were similar to those in PB rather than in BM. The B cells in CB contained an increased proportion of B cells expressing a high level of CD24 and a low proportion of B cells expressing CD27, pointing to the presence of circulating CD24high immature transitional and CD27– naive B cells. CD40-mediated activation of ERK and p38 was also minimal in these B cells of CB. These findings may account for the functional defects of B cells in transplanted CB.

Key Words: B-cell antigen receptor • CD40 • signal transduction • transitional B cells