INHIBITION OF INTERLEUKIN 2 RECEPTOR EXPRESSION IN NORMAL HUMAN T CELLS BY CYCLOSPORINE

1992 ◽  
Vol 53 (1) ◽  
pp. 146-150 ◽  
Author(s):  
BAOGUI LI ◽  
PRABODH K. SEHAJPAL ◽  
AJIT SUBRAMANIAM ◽  
ANTONIO JOSEPH ◽  
KURT H. STENZEL ◽  
...  
Keyword(s):  
T Cells ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Interleukin 2 Receptor ◽  
Human T Cells ◽  
Normal Human

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.

1,25-Dihydroxyvitamin-D3 regulation of interleukin-2 and interleukin-2 receptor levels and gene expression in human T cells

1989 ◽  
Vol 26 (10) ◽  
pp. 979-984 ◽  
Author(s):  
Stanley C. Jordan ◽  
Mieko Toyoda ◽  
John Prehn ◽  
Jacques M. Lemire ◽  
Rebecca Sakai ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Interleukin 2 ◽  
Dihydroxyvitamin D3 ◽  
Interleukin 2 Receptor ◽  
1,25 Dihydroxyvitamin D3 ◽  
Human T Cells

Enhancement of the interleukin 2 receptor expression on T cells by multiple B-lymphotropic lymphokines

1987 ◽  
Vol 15 (3) ◽  
pp. 249-253 ◽  
Author(s):  
Takafumi Noma ◽  
Tatsunobu Mizuta ◽  
Anders Rosén ◽  
Toshio Hirano ◽  
Tadamitsu Kishimoto ◽  
...  
Keyword(s):  
T Cells ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Interleukin 2 Receptor

scholarly journals Expression of NFAT-family proteins in normal human T cells.

1997 ◽  
Vol 17 (5) ◽  
pp. 2475-2484 ◽  
Author(s):  
L Lyakh ◽  
P Ghosh ◽  
N R Rice
Keyword(s):  
T Cells ◽  
Dna Binding ◽  
Interleukin 2 ◽  
Binding Assays ◽  
Myristate Acetate ◽  
Human T Cells ◽  
Specific Antisera ◽  
Predominant Form ◽  
Normal Human ◽  
Size Heterogeneity

NFAT proteins constitute a family of transcription factors involved in mediating signal transduction. Using a panel of specific antisera in immunoprecipitation assays, we found that NFATp (135 kDa) is constitutively expressed in normal human T cells, while synthesis of NFATc (predominant form of 86 kDa) is induced by ionomycin treatment. NFAT4/x was very weakly expressed in unstimulated cells, and its level did not increase upon treatment with activating agents. NFAT3 protein was not observed under any conditions. Higher-molecular-weight species of NFATc (of 110 and 140 kDa) were also detected. In addition, translation of NFATc mRNA apparently initiates at two different AUG codons, giving rise to proteins that differ in size by 36 amino acids. Additional size heterogeneity of both NFATc and NFATp results from phosphorylation. In contrast to ionomycin treatment, exposure of cells to phorbol myristate acetate (PMA) plus anti-CD28 did not induce NFATc, indicating that under these conditions, interleukin-2 synthesis by these cells is apparently independent of NFATc. In DNA binding assays, both PMA plus anti-CD28 and PMA plus ionomycin resulted in nuclear NFAT. Surprisingly, the PMA-ionomycin-induced synthesis of NFATc that was detected by immunoprecipitation was not mirrored in the DNA binding assays: nearly all of the activity was due to NFATp. This is the first study of expression of all family members at the protein level in normal human T cells.

6.7 Different rates of interleukin 2 receptor expression by ovine γ/δ and α/β T cells

1993 ◽  
Vol 39 (1-3) ◽  
pp. 109-114 ◽  
Author(s):  
Raymond Bujdoso ◽  
Brett.T. Lund ◽  
Carys W. Evans ◽  
Ian McConnell
Keyword(s):  
T Cells ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Interleukin 2 Receptor

Interleukin 2 receptor expression by T cells in human aging

1989 ◽  
Vol 124 (2) ◽  
pp. 278-291 ◽  
Author(s):  
Frank M. Orson ◽  
Constantine K. Saadeh ◽  
Dorothy E. Lewis ◽  
David L. Nelson
Keyword(s):  
T Cells ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Human Aging ◽  
Interleukin 2 Receptor

scholarly journals 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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