scholarly journals An Evaluation of T‐Cell Functionality After Flow Cytometry Sorting Revealed p38 MAPK Activation

2020 ◽  
Vol 97 (2) ◽  
pp. 171-183 ◽  
Author(s):  
Immanuel Andrä ◽  
Hanna Ulrich ◽  
Susi Dürr ◽  
Dominik Soll ◽  
Lynette Henkel ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cell ◽  
P38 Mapk ◽  
Mapk Activation ◽  
Cell Functionality ◽  
Flow Cytometry Sorting

T-Cell Receptor Signaling Pathway Exerts a Negative Control on Thrombin-Mediated Increase in [Ca2+]i and p38 MAPK Activation in Jurkat T Cells: Implication of the Tyrosine Kinase p56Lck

Blood ◽  
1998 ◽  
Vol 91 (11) ◽  
pp. 4232-4241 ◽  
Author(s):  
Laurence Maulon ◽  
Sandrine Guérin ◽  
Jean-Ehrland Ricci ◽  
Dariush FarahiFar ◽  
Jean-Philippe Breittmayer ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Phosphorylation ◽  
P38 Mapk ◽  
Cell Lines ◽  
Cell Receptor ◽  
Negative Control ◽  
Mapk Activation ◽  
Jurkat T Cell ◽  
Receptor Signaling Pathway ◽  
T Cell Lines

Abstract Activation of the mitogen-activated protein kinase (Erk) and c-Jun terminal kinase is a well-documented mechanism for the seven transmembrane spanning receptors. We have previously shown that thrombin stimulation of the T-leukemic cell line Jurkat induced a transient increase in [Ca2+]i and tyrosine phosphorylation of several cellular proteins. Here, we have analyzed p42-44 MAPK, JNK and p38 MAPK activation using Jurkat T-cell lines deficient in either the tyrosine kinase p56Lck (JCaM1) or the tyrosine phosphatase CD45 (J45.01). Our results demonstrate that p56Lck and CD45 exert a negative control on thrombin-induced p38 MAPK activation and [Ca2+]i release in Jurkat cells. Thrombin receptor expression was identical on the different cell lines as assessed by FACS analysis. Tyrosine phosphorylation of p38 MAPK was drastically increased after thrombin stimulation of JCaM1 or J45.01 cells, as compared with parental cells (JE6.1). P42-44 MAPK and JNK activity also enhanced after thrombin treatment of JE6.1 and JCaM1 cell lines, whereas basal kinase activity was higher in J45.01 cells and was not further stimulated by thrombin. Thrombin and thrombin receptor agonist peptide-induced [Ca2+]imobilization paralleled p38 MAPK activation in JCaM1 and J45.01 cells. Moreover, reconstitution of J45.01 and JCaM1 cell lines with either CD45 or Lck is accompanied by restoration of a normal thrombin-induced [Ca2+]i response and p38MAPK phosphorylation. These data show that a component of the T-cell receptor signaling pathway exerts a negative control on thrombin-induced responses in Jurkat T cells. Accordingly, we found that thrombin enhanced tyrosine phosphorylation of p56Lck and decreased p56Lck kinase activity in J45.01 cells. Our results are consistent with a negative role for p56Lck on thrombin-induced [Ca2+]i release and p38 MAPK activation in Jurkat T-cell lines.

scholarly journals Shockwaves increase T-cell proliferation and IL-2 expression through ATP release, P2X7 receptors, and FAK activation

2010 ◽  
Vol 298 (3) ◽  
pp. C457-C464 ◽  
Author(s):  
Tiecheng Yu ◽  
Wolfgang G. Junger ◽  
Changji Yuan ◽  
An Jin ◽  
Yi Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
P38 Mapk ◽  
Cell Function ◽  
Receptor Activation ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
T Cell Proliferation ◽  
P2x7 Receptors ◽  
Mapk Activation

Shockwaves elicited by transient pressure disturbances are used to treat musculoskeletal disorders. Previous research has shown that shockwave treatment affects T-cell function, enhancing T-cell proliferation and IL-2 expression by activating p38 mitogen-activated protein kinase (MAPK) signaling. Here we investigated the signaling pathway by which shockwaves mediate p38 MAPK phosphorylation. We found that shockwaves at an intensity of 0.18 mJ/mm2induce the release of extracellular ATP from human Jurkat T-cells at least in part by affecting cell viability. ATP released into the extracellular space stimulates P2X7-type purinergic receptors that induce the activation of p38 MAPK and of focal adhesion kinase (FAK) by phosphorylation on residues Tyr397 and Tyr576/577. Elimination of released ATP with apyrase or inhibition of P2X7 receptors with the antagonists KN-62 or suramin significantly weakens FAK phosphorylation, p38 MAPK activation, IL-2 expression, and T-cell proliferation. Conversely, addition of exogenous ATP causes phosphorylation of FAK and p38 MAPK. Silencing of FAK expression also reduces these cell responses to shockwave treatment. We conclude that shockwaves enhance p38 MAPK activation, IL-2 expression, and T-cell proliferation via the release of cellular ATP and feedback mechanisms that involve P2X7 receptor activation and FAK phosphorylation.

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.

T-Cell Receptor Signaling Pathway Exerts a Negative Control on Thrombin-Mediated Increase in [Ca2+]i and p38 MAPK Activation in Jurkat T Cells: Implication of the Tyrosine Kinase p56Lck

Blood ◽  
1998 ◽  
Vol 91 (11) ◽  
pp. 4232-4241 ◽  
Author(s):  
Laurence Maulon ◽  
Sandrine Guérin ◽  
Jean-Ehrland Ricci ◽  
Dariush FarahiFar ◽  
Jean-Philippe Breittmayer ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Phosphorylation ◽  
P38 Mapk ◽  
Cell Lines ◽  
Cell Receptor ◽  
Negative Control ◽  
Mapk Activation ◽  
Jurkat T Cell ◽  
Receptor Signaling Pathway ◽  
T Cell Lines

Activation of the mitogen-activated protein kinase (Erk) and c-Jun terminal kinase is a well-documented mechanism for the seven transmembrane spanning receptors. We have previously shown that thrombin stimulation of the T-leukemic cell line Jurkat induced a transient increase in [Ca2+]i and tyrosine phosphorylation of several cellular proteins. Here, we have analyzed p42-44 MAPK, JNK and p38 MAPK activation using Jurkat T-cell lines deficient in either the tyrosine kinase p56Lck (JCaM1) or the tyrosine phosphatase CD45 (J45.01). Our results demonstrate that p56Lck and CD45 exert a negative control on thrombin-induced p38 MAPK activation and [Ca2+]i release in Jurkat cells. Thrombin receptor expression was identical on the different cell lines as assessed by FACS analysis. Tyrosine phosphorylation of p38 MAPK was drastically increased after thrombin stimulation of JCaM1 or J45.01 cells, as compared with parental cells (JE6.1). P42-44 MAPK and JNK activity also enhanced after thrombin treatment of JE6.1 and JCaM1 cell lines, whereas basal kinase activity was higher in J45.01 cells and was not further stimulated by thrombin. Thrombin and thrombin receptor agonist peptide-induced [Ca2+]imobilization paralleled p38 MAPK activation in JCaM1 and J45.01 cells. Moreover, reconstitution of J45.01 and JCaM1 cell lines with either CD45 or Lck is accompanied by restoration of a normal thrombin-induced [Ca2+]i response and p38MAPK phosphorylation. These data show that a component of the T-cell receptor signaling pathway exerts a negative control on thrombin-induced responses in Jurkat T cells. Accordingly, we found that thrombin enhanced tyrosine phosphorylation of p56Lck and decreased p56Lck kinase activity in J45.01 cells. Our results are consistent with a negative role for p56Lck on thrombin-induced [Ca2+]i release and p38 MAPK activation in Jurkat T-cell lines.

scholarly journals Hypertonic Stress Increases T Cell Interleukin-2 Expression through a Mechanism That Involves ATP Release, P2 Receptor, and p38 MAPK Activation

2002 ◽  
Vol 278 (7) ◽  
pp. 4590-4596 ◽  
Author(s):  
William H. Loomis ◽  
Sachiko Namiki ◽  
Rennolds S. Ostrom ◽  
Paul A. Insel ◽  
Wolfgang G. Junger
Keyword(s):  
T Cell ◽  
P38 Mapk ◽  
Interleukin 2 ◽  
Atp Release ◽  
P2 Receptor ◽  
Mapk Activation ◽  
Hypertonic Stress

scholarly journals Conventional and Computational Flow Cytometry Analyses Reveal Sustained Human Intrathymic T Cell Development From Birth Until Puberty

2020 ◽  
Vol 11 ◽  
Author(s):  
Marieke Lavaert ◽  
Brecht Valcke ◽  
Bart Vandekerckhove ◽  
Georges Leclercq ◽  
Kai Ling Liang ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cell ◽  
T Cell Development ◽  
Cell Development
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