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CM1 ligation initiates apoptosis in a caspase 8-dependent manner in Ramos cells and in a mitochondria-controlled manner in Raji cells

Authors
Kim, DHur, DYKim, YSLee, KLee, YCho, DKang, JSKim, YIHahm, EYang, YYoon, SKim, SLee, WBPark, HYKim, YBHwang, YIChang, KYLee, WJ
Issue Date
Jul-2002
Publisher
ELSEVIER SCIENCE INC
Keywords
CM1; apoptosis; Ramos (centroblasts); Raji (centrocytes)
Citation
HUMAN IMMUNOLOGY, v.63, no.7, pp 576 - 587
Pages
12
Journal Title
HUMAN IMMUNOLOGY
Volume
63
Number
7
Start Page
576
End Page
587
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/16410
DOI
10.1016/S0198-8859(02)00405-6
ISSN
0198-8859
1879-1166
Abstract
Burkitt lymphoma (BL) is a tumor with the characteristics of germinal center B cells. We previously reported that the CM1 (centrocyte/-blast marker 1) molecule is expressed only in germinal center B cells, specifically, in a subpopulation of centroblasts and centrocytes. In the present study, we investigated the apoptosis induced by anti-CM1 in the Ramos and Raji human BL cell lines. The Ramos is protected from apoptosis by the crosslinking of sIgM and the calcium ionophore by the ligation of CD40 with anti-CD40 monoclonal antibodies (mAb) or soluble CD40 ligand (sCD40L). In this investigation on the effect of CM1 on apoptosis in BL cell lines, we found that ceIlular signaling by CM1 induces apoptosis and decreases cell viability, in BL cell lines cultured for 24 hours with protein-G, agarose beads conjugated anti-CM1 mAb. Stimulation by CD40 ligated with sCD40L protected Raji cells from CM1-induced apoptosis, but did nor protect Ramos cells. Furthermore, after anti-CM1 mAb stimulation, CD95 expression was upregulated and CD40 expression was unaltered or slightly decreased in Ramos cells, whereas CD95 was down regulated and CD40 was slightly upregulated in Raji cells. The engagement of CD40 by sCD40L enhanced CD95 expression, but the level of CM1 expression was unchanged in Ramos. However, sCD40L downregulated both CD95 and CM1 expression in Raji. In addition, the caspase-8 specific inhibitor blocked CM1-induced apoptosis in Ramos cells, but not in Raji cells. Increased mitochondrial membrane permeabilization was observed only in Raji cells. Moreover, the effector caspase inhibitor, z-DEVD, blocked CM1-mediated apoptosis in both cell lines. We found that CM1-induced apoptosis is achieved via different initiation pathways, which arc celt-type dependent. (C) American Society for Histocompatibility and Immunogenetics, 2002. Published by Elsevier Science Inc.
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