scholarly journals Supplementation with selenium and human immune cell functions: I. Effect on lymphocyte proliferation and interleukin 2 receptor expression

1994 ◽  
Vol 46 (1-2) ◽  
pp. 183-183 ◽  
Author(s):  
Martin Roy ◽  
Lidia Kiremidjian-Schumacher ◽  
Harvey I. Wishe ◽  
Martin W. Cohen ◽  
Günther Stotzky
Keyword(s):  
Lymphocyte Proliferation ◽  
Immune Cell ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Cell Functions ◽  
Interleukin 2 Receptor ◽  
Human Immune

Selenium and Immune Cell Functions. I. Effect on Lymphocyte Proliferation and Production of Interleukin 1 and Interleukin 2

1990 ◽  
Vol 193 (2) ◽  
pp. 136-142 ◽  
Author(s):  
L. Kiremidjian-Schumacher ◽  
M. Roy ◽  
H. I. Wishe ◽  
M. W. Cohen ◽  
G. Stotzky
Keyword(s):  
Lymphocyte Proliferation ◽  
Immune Cell ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Cell Functions

Diltiazem inhibits transferrin receptor expression and causes G1 arrest in normal and neoplastic T cells

1986 ◽  
Vol 6 (12) ◽  
pp. 4244-4250
Author(s):  
L M Neckers ◽  
S Bauer ◽  
R C McGlennen ◽  
J B Trepel ◽  
K Rao ◽  
...  
Keyword(s):  
T Cells ◽  
Transferrin Receptor ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Calcium Flux ◽  
G1 Arrest ◽  
Receptor Mrna ◽  
Interleukin 2 Receptor ◽  
Transferrin Receptor Expression ◽  
Malignant T Cells

Transferrin receptor expression is essential for the proliferation of both normal and malignant T cells. While transferrin receptor expression in normal T cells is tightly coupled to interleukin-2 receptor expression, transferrin receptor expression in malignant cells is usually constitutive and is released from this constraint. Temporally, the appearance of these membrane receptors is preceded by changes in the expression of the proto-oncogenes c-myc and c-myb. In addition, although an increase in the level of intracellular free calcium occurs early in the sequence of T-cell activation, the activation events dependent on this calcium flux have not been resolved. In the present study we report that diltiazem, an ion channel-blocking agent that inhibits calcium influx, arrested the growth in vitro of both normal and malignant human T cells in the G1 phase of the cell cycle. However, diltiazem did not inhibit the expression of c-myc or interleukin-2 receptor mRNA and protein in normal mitogen-activated T cells or the constitutive expression of c-myc and c-myb mRNA in malignant T cells (T acute lymphoblastic leukemia cells). In contrast, diltiazem prevented the induction of transferrin receptor (mRNA and protein) in normal T cells and caused a progressive loss of transferrin receptor (mRNA and protein) in malignant T cells. These data demonstrate that diltiazem can dissociate several growth-related processes normally occurring in G1 and thereby disrupt the biochemical cascade leading to cell proliferation.

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