HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Taguchi, T. Articles by Fujimoto, J. Search for Related Content PubMed PubMed Citation Articles by Taguchi, T. Articles by Fujimoto, J. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene

Pre-B Cell Antigen Receptor-Mediated Signal Inhibits CD24-Induced Apoptosis in Human Pre-B Cells¹

Tomoko Taguchi^*,, Nobutaka Kiyokawa^2,*, Kenichi Mimori^*, Toyo Suzuki^*, Takaomi Sekino^*, Hideki Nakajima^*, Masahiro Saito^*, Yohko U. Katagiri^*, Nobutake Matsuo, Yoshinobu Matsuo, Hajime Karasuyama^¶ and Junichiro Fujimoto^*

^* Department of Developmental Biology, National Research Institute for Child Health and Development, Tokyo, Japan; Department of Pediatrics, School of Medicine, Keio University, Tokyo, Japan; National Center for Child Health and Development, Tokyo, Japan; Fujisaki Cell Center, Hayashibara Biochemical Labs Inc., Okayama, Japan; and ^¶ Department of Immune Regulation, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan

We previously reported that the cross-linking of cluster of differentiation (CD)24 induces apoptosis in Burkitt’s lymphoma cells and that this phenomenon can be enhanced by a B cell Ag receptor (BCR)-mediated signal. In this study, we extend our previous observation and report that CD24 also mediated apoptosis in human precursor-B acute lymphoblastic leukemia cell lines in the pro-B and pre-B stages accompanying activation of multiple caspases. Interestingly, simultaneous cross-linking of pre-BCR clearly inhibited CD24-mediated apoptosis in pre-B cells. We also observed that mitogen-activated protein kinases (MAPKs) were involved in the regulation of this apoptotic process. Pre-BCR cross-linking induced prompt and strong activation of extracellular signal-regulated kinase 1, whereas CD24 cross-linking induced the sustained activation of p38 MAPK, following weak extracellular signal-regulated kinase 1 activation. SC68376, a specific inhibitor of p38 MAPK, inhibited apoptosis induction by CD24 cross-linking, whereas anisomycin, an activator of p38 MAPK, enhanced the apoptosis. In addition, PD98059, a specific inhibitor of MEK-1, enhanced apoptosis induction by CD24 cross-linking and reduced the antiapoptotic effects of pre-BCR cross-linking. Collectively, whether pre-B cells survive or die may be determined by the magnitude of MAPK activation, which is regulated by cell surface molecules. Our findings should be important to understanding the role of CD24-mediated cell signaling in early B cell development.

This article has been cited by other articles:

				E. Sagiv, A. Starr, U. Rozovski, R. Khosravi, P. Altevogt, T. Wang, and N. Arber Targeting CD24 for Treatment of Colorectal and Pancreatic Cancer by Monoclonal Antibodies or Small Interfering RNA Cancer Res., April 15, 2008; 68(8): 2803 - 2812. [Abstract] [Full Text] [PDF]

				Y. Wang, P. H. Dennehy, H. L. Keyserling, K. Tang, J. R. Gentsch, R. I. Glass, and B. Jiang Rotavirus Infection Alters Peripheral T-Cell Homeostasis in Children with Acute Diarrhea J. Virol., April 15, 2007; 81(8): 3904 - 3912. [Abstract] [Full Text] [PDF]

				K. C. Jung, W. S. Park, H. J. Kim, E. Y. Choi, M.-C. Kook, H.-W. Lee, and Y. Bae TCR-Independent and Caspase-Independent Apoptosis of Murine Thymocytes by CD24 Cross-Linking J. Immunol., January 15, 2004; 172(2): 795 - 802. [Abstract] [Full Text] [PDF]

				J. Soret, M. Gabut, C. Dupon, G. Kohlhagen, J. Stevenin, Y. Pommier, and J. Tazi Altered Serine/Arginine-Rich Protein Phosphorylation and Exonic Enhancer-Dependent Splicing in Mammalian Cells Lacking Topoisomerase I Cancer Res., December 1, 2003; 63(23): 8203 - 8211. [Abstract] [Full Text] [PDF]