Suppression of Interleukin-2 Receptor Expression on Mouse CD4+T Cells by Bovine κ-Caseinoglycopeptide

1996 ◽  
Vol 60 (6) ◽  
pp. 1017-1019 ◽  
Author(s):  
Hajime Otani ◽  
Yasuhiro Horimoto ◽  
Makoto Monnai
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Interleukin 2 Receptor

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.

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

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

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.

scholarly journals Induction of severe granulomatous experimental autoimmune thyroiditis in mice by effector cells activated in the presence of anti-interleukin 2 receptor antibody.

1991 ◽  
Vol 173 (4) ◽  
pp. 899-912 ◽  
Author(s):  
H Braley-Mullen ◽  
G C Sharp ◽  
J T Bickel ◽  
M Kyriakos
Keyword(s):  
T Cells ◽  
Autoimmune Thyroiditis ◽  
Cd4 T Cells ◽  
Mononuclear Cells ◽  
Interleukin 2 ◽  
Cell Activity ◽  
Experimental Autoimmune Thyroiditis ◽  
Interleukin 2 Receptor ◽  
Cells Cultured ◽  
Experimental Autoimmune

Spleen cells from CBA/J mice immunized with mouse thyroglobulin (MTg) and the adjuvant lipopolysaccharide induce experimental autoimmune thyroiditis (EAT) after transfer to recipient mice if they are first activated in vitro with MTg. EAT induced by cells cultured with MTg is generally moderate in severity and is characterized by a thyroid infiltration consisting primarily of mononuclear cells. Addition of the anti-interleukin 2 receptor (IL-2R) monoclonal antibodies (mAbs) M7/20, 3C7, or 7D4 to spleen cell cultures with MTg resulted in a cell population capable of inducing a more severe type of EAT characterized by extensive follicular destruction, granuloma formation, and the presence of multinucleated giant cells. Recipients of cells cultured with MTg and anti-IL-2R mAb also had higher anti-MTg autoantibody responses than recipients of cells cultured with MTg alone. Activation of cells capable of transferring severe granulomatous EAT and increased anti-MTg autoantibody responses required both MTg and M7/20 in culture and required addition of M7/20 within the first 8 h of the 72-h culture period. CD4+ T cells were required for the expression of both the severe granulomatous EAT lesions and the mononuclear cell infiltrates typically observed in murine EAT. The increased anti-MTg autoantibody responses in recipients of cells cultured with MTg and anti-IL-2R mAbs were not restricted to a particular immunoglobulin G (IgG) subclass and included antibody of the IgG1, IgG2A, and IgG2B subclasses. These results suggest that a subset of CD4+ T cells capable of inducing severe granulomatous EAT and increased anti-MTg autoantibody responses is preferentially activated when cells are cultured in the presence of anti-IL-2R mAb. Anti-IL-2R mAb may either prevent activation of cells that induce classical lymphocytic EAT or prevent activation of cells that normally function to downregulate EAT effector T cell activity.

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