A p38 MAP kinase inhibitor SB203580 inhibits CD28-dependent T cell proliferation and IL-2 production

1997 ◽  
Vol 25 (2) ◽  
pp. 304S-304S ◽  
Author(s):  
STEPHEN G. WARD ◽  
RICHARD V. PARRY ◽  
JANE MATTHEWS ◽  
LUKE O'NEILL
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Map Kinase ◽  
Kinase Inhibitor ◽  
P38 Map Kinase ◽  
T Cell Proliferation

scholarly journals Blockade of PD-1 or p38 MAP kinase signaling enhances senescent human CD8+T-cell proliferation by distinct pathways

2015 ◽  
Vol 45 (5) ◽  
pp. 1441-1451 ◽  
Author(s):  
Sian M. Henson ◽  
Richard Macaulay ◽  
Natalie E. Riddell ◽  
Craig J. Nunn ◽  
Arne N. Akbar
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Map Kinase ◽  
Cd8 T Cell ◽  
P38 Map Kinase ◽  
T Cell Proliferation ◽  
Kinase Signaling ◽  
Map Kinase Signaling

scholarly journals IL-7 promotes T cell proliferation through destabilization of p27Kip1

2006 ◽  
Vol 203 (3) ◽  
pp. 573-582 ◽  
Author(s):  
Wen Qing Li ◽  
Qiong Jiang ◽  
Eiman Aleem ◽  
Philipp Kaldis ◽  
Annette R. Khaled ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Kinase Inhibitor ◽  
S Phase ◽  
T Cell Proliferation ◽  
G1 Arrest ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Survival Effect ◽  
Interfering Rna

Interleukin (IL)-7 is required for survival and homeostatic proliferation of T lymphocytes. The survival effect of IL-7 is primarily through regulation of Bcl-2 family members; however, the proliferative mechanism is unclear. It has not been determined whether the IL-7 receptor actually delivers a proliferative signal or whether, by promoting survival, proliferation results from signals other than the IL-7 receptor. We show that in an IL-7–dependent T cell line, cells protected from apoptosis nevertheless underwent cell cycle arrest after IL-7 withdrawal. This arrest was accompanied by up-regulation of the cyclin-dependent kinase inhibitor p27Kip1 through a posttranslational mechanism. Overexpression of p27Kip1 induced G1 arrest in the presence of IL-7, whereas knockdown of p27Kip1 by small interfering RNA promoted S phase entry after IL-7 withdrawal. CD4 or CD8 T cells transferred into IL-7–deficient hosts underwent G1 arrest, whereas 27Kip1-deficient T cells underwent proliferation. We observed that IL-7 withdrawal activated protein kinase C (PKC)θ and that inhibition of PKCθ with a pharmacological inhibitor completely blocked the rise of p27Kip1 and rescued cells from G1 arrest. The conventional pathway to breakdown of p27Kip1 is mediated by S phase kinase-associated protein 2; however, our evidence suggests that PKCθ acts via a distinct, unknown pathway inducing G1 arrest after IL-7 withdrawal from T cells. Hence, IL-7 maintains T cell proliferation through a novel pathway of p27Kip1 regulation.

scholarly journals Shock Waves Increase T-cell Proliferation or IL-2 Expression by Activating p38 MAP Kinase

2004 ◽  
Vol 36 (11) ◽  
pp. 741-748 ◽  
Author(s):  
Tie-Cheng Yu ◽  
Yi Liu ◽  
Yan Tan ◽  
Yanfang Jiang ◽  
Xueqing Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Shock Waves ◽  
P38 Mapk ◽  
Cell Function ◽  
P38 Map Kinase ◽  
Mitogen Activated Protein Kinase ◽  
T Cell Proliferation ◽  
Mapk Activation ◽  
T Cell Function

Abstract Shock waves were elicited by transient pressure disturbances, which could be used to treat musculoskeletal disorders. In present studies, we investigated whether the low-density shock waves (LDSWs), which are able to damage plasma membrane without impairing the vimentin or other organelles, might augment T-cell proliferation as well as IL-2 expression, and if mitogen activated protein kinase p38 (p38 MAPK) might be an underlying mechanism through which the LDSWs enhanced T-cell function. We found that the LDSWs increased activation of p38 MAPK in Jurkat T cells. The LDSWs alone didn't result in the T-cell proliferation and IL-2 expression. However, in combination with other stimuli, LDSWs could augment the T-cell proliferation and IL-2 expression. Inhibition of p38 MAPK using SB203580 reduced the stimulatory effects of the LDSWs, which indicated that the LDSWs enhanced IL-2 expression through a mechanism that involved p38 MAPK activation. We concluded that the p38 MAPK activation played a key role in the regulation of T cell function by the LDSWs.

Interleukin-7 induces T cell proliferation in the absence of Erk/MAP kinase activity

1996 ◽  
Vol 26 (11) ◽  
pp. 2717-2723 ◽  
Author(s):  
James B. Crawley ◽  
Joannie Willcocks ◽  
Brian M. J. Foxwell
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Map Kinase ◽  
Kinase Activity ◽  
T Cell Proliferation ◽  
Interleukin 7
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