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CD6 ligation modulates the Bcl-2/Bax ratio and protects chronic lymphocytic
leukemia B cells from apoptosis induced by anti-IgM
LM Osorio, A De Santiago, M Aguilar-Santelises, H Mellstedt and M Jondal
Department of Toxicology, Karolinska Institute, Stockholm, Sweden.
CD6 and CD5 belong to a scavenger-receptor cysteine-rich (SRCR) super
family of membrane glycoproteins that are expressed on chronic lymphocytic
leukemia B (B-CLL) cells, normal T cells, and a small subset of normal B
cells. CD6 configures in the membrane in relation to the cellular
activation level and can act as a coreceptor for T-cell activation. We have
examined a group of progressive and nonprogressive B-CLL cells. Most B-CLL
cells were positive for CD6 and the expression of CD6 was increased after
activation with Staphylococcus aureus Cowan I plus interleukin-2 or
12-O-tetradecanoylphorbol 13-acetate, although anti-CD6 antibodies did not
increase proliferative responses to these stimuli. However, anti-CD6
stimulation was found to protect against anti-IgM-induced apoptosis in
B-CLL. bax(alpha) upregulation and bcl-2 downregulation were found in
anti-IgM- and glucocorticoid (GCC)-induced apoptotic cells, respectively.
Furthermore, CD6 cross-linking downregulated bax(alpha) mRNA levels in
anti-IgM-treated cells, resulting in an increased bcl-2/bax(alpha) ratio.
CD6 activation also prevented bcl-2 mRNA downregulation and apoptosis
induced by GCC in one of six GCC-sensitive patients. These data suggest
that an interaction between CD6 and its ligand might contribute to B-CLL
survival through the modulation of the Bcl-2/Bax ratio.
Volume 89,
Issue 8,
pp. 2833-2841,
04/15/1997
Copyright © 1997 by The American Society of Hematology
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