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

Daejin Kim, Dae Young Hur, Yeong Seok Kim, Kyungmi Lee, Youngseon Lee, Daeho Cho, Jae Seung Kang, Young In Kim Hoehamer, Eunsil Hahm, Yoolhee Yang, Suyoung Yoon, Seonghan Kim, Won Bok Lee, Hae Young Park, Yoon Berm Kim, Young Il Hwang, Ka Y. Chang, Wang Jae Lee

Research output: Contribution to journalArticle

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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 cellular 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 not 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 downregulated 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 are cell-type dependent.

Original languageEnglish (US)
Pages (from-to)576-587
Number of pages12
JournalHuman Immunology
Volume63
Issue number7
DOIs
StatePublished - Jul 6 2002

Fingerprint

Caspase 8
Ligation
Mitochondria
Apoptosis
CD40 Ligand
Burkitt Lymphoma
Cell Line
Germinal Center
Monoclonal Antibodies
B-Lymphocytes
Down-Regulation
Effector Caspases
Caspase Inhibitors
Calcium Ionophores
Mitochondrial Membranes
Sepharose
Cell Survival

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

CM1 ligation initiates apoptosis in a caspase 8-dependent manner in Ramos cells and in a mitochondria-controlled manner in Raji cells. / Kim, Daejin; Hur, Dae Young; Kim, Yeong Seok; Lee, Kyungmi; Lee, Youngseon; Cho, Daeho; Kang, Jae Seung; Kim Hoehamer, Young In; Hahm, Eunsil; Yang, Yoolhee; Yoon, Suyoung; Kim, Seonghan; Lee, Won Bok; Park, Hae Young; Kim, Yoon Berm; Hwang, Young Il; Chang, Ka Y.; Lee, Wang Jae.

In: Human Immunology, Vol. 63, No. 7, 06.07.2002, p. 576-587.

Research output: Contribution to journalArticle

Kim, D, Hur, DY, Kim, YS, Lee, K, Lee, Y, Cho, D, Kang, JS, Kim Hoehamer, YI, Hahm, E, Yang, Y, Yoon, S, Kim, S, Lee, WB, Park, HY, Kim, YB, Hwang, YI, Chang, KY & Lee, WJ 2002, 'CM1 ligation initiates apoptosis in a caspase 8-dependent manner in Ramos cells and in a mitochondria-controlled manner in Raji cells', Human Immunology, vol. 63, no. 7, pp. 576-587. https://doi.org/10.1016/S0198-8859(02)00405-6
Kim, Daejin ; Hur, Dae Young ; Kim, Yeong Seok ; Lee, Kyungmi ; Lee, Youngseon ; Cho, Daeho ; Kang, Jae Seung ; Kim Hoehamer, Young In ; Hahm, Eunsil ; Yang, Yoolhee ; Yoon, Suyoung ; Kim, Seonghan ; Lee, Won Bok ; Park, Hae Young ; Kim, Yoon Berm ; Hwang, Young Il ; Chang, Ka Y. ; Lee, Wang Jae. / CM1 ligation initiates apoptosis in a caspase 8-dependent manner in Ramos cells and in a mitochondria-controlled manner in Raji cells. In: Human Immunology. 2002 ; Vol. 63, No. 7. pp. 576-587.
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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 cellular 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 not 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 downregulated 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 are cell-type dependent.",
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T1 - CM1 ligation initiates apoptosis in a caspase 8-dependent manner in Ramos cells and in a mitochondria-controlled manner in Raji cells

AU - Kim, Daejin

AU - Hur, Dae Young

AU - Kim, Yeong Seok

AU - Lee, Kyungmi

AU - Lee, Youngseon

AU - Cho, Daeho

AU - Kang, Jae Seung

AU - Kim Hoehamer, Young In

AU - Hahm, Eunsil

AU - Yang, Yoolhee

AU - Yoon, Suyoung

AU - Kim, Seonghan

AU - Lee, Won Bok

AU - Park, Hae Young

AU - Kim, Yoon Berm

AU - Hwang, Young Il

AU - Chang, Ka Y.

AU - Lee, Wang Jae

PY - 2002/7/6

Y1 - 2002/7/6

N2 - 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 cellular 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 not 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 downregulated 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 are cell-type dependent.

AB - 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 cellular 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 not 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 downregulated 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 are cell-type dependent.

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