scholarly journals The role of the ERK MAP kinase pathway in CD4 T cell proliferation and differentiation

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Chiung‐Fang Chang ◽  
Warren N. D'souza ◽  
Saswata Talukdar ◽  
Stephen M. Hedrick
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Map Kinase ◽  
Cd4 T Cell ◽  
T Cell Proliferation ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Map Kinase Pathway ◽  
Kinase Pathway

scholarly journals Costimulation by B7 Modulates Specificity of Cytotoxic T Lymphocytes: A Missing Link That Explains Some Bystander T Cell Activation

1997 ◽  
Vol 186 (10) ◽  
pp. 1787-1791 ◽  
Author(s):  
Pan Zheng ◽  
Yang Liu
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
Influenza Virus ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
T Cell Proliferation ◽  
Target Cells ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

It has been proposed that some bystander T cell activation may in fact be due to T cell antigen receptor (TCR) cross-reactivity that is too low to be detected by the effector cytotoxic T lymphocyte (CTL). However, this hypothesis is not supported by direct evidence since no TCR ligand is known to induce T cell proliferation and differentiation without being recognized by the effector CTL. Here we report that transgenic T cells expressing a T cell receptor to influenza virus A/NT/68 nucleoprotein (NP) 366-374:Db complexes clonally expand and become effector CTLs in response to homologous peptides from either A/PR8/34 (H1N1), A/AA/60 (H2N2), or A/NT/68 (H3N2). However, the effector T cells induced by each of the three peptides kill target cells pulsed with NP peptides from the H3N2 and H2N2 viruses, but not from the H1N1 virus. Thus, NP366–374 from influenza virus H1N1 is the first TCR ligand that can induce T cell proliferation and differentiation without being recognized by CTLs. Since induction of T cell proliferation was mediated by antigen-presenting cells that express costimulatory molecules such as B7, we investigated if cytolysis of H1N1 NP peptide–pulsed targets can be restored by expressing B7-1 on the target cells. Our results revealed that this is the case. These data demonstrated that costimulatory molecule B7 modulates antigen specificity of CTLs, and provides a missing link that explains some of the bystander T cell activation.

scholarly journals Extracellular Zinc Triggers ERK-dependent Activation of Na+/H+Exchange in Colonocytes Mediated by the Zinc-sensing Receptor

2004 ◽  
Vol 279 (50) ◽  
pp. 51804-51816 ◽  
Author(s):  
Hagit Azriel-Tamir ◽  
Haleli Sharir ◽  
Betty Schwartz ◽  
Michal Hershfinkel
Keyword(s):  
Cell Proliferation ◽  
Map Kinase ◽  
Ph Homeostasis ◽  
Ht29 Cells ◽  
Intracellular Release ◽  
Map Kinase Pathway ◽  
Zinc Sensing ◽  
Multiple Signaling ◽  
Kinase Pathway

Extracellular zinc promotes cell proliferation and its deficiency leads to impairment of this process, which is particularly important in epithelial cells. We have recently characterized a zinc-sensing receptor (ZnR) linking extracellular zinc to intracellular release of calcium. In the present study, we addressed the role of extracellular zinc, acting via the ZnR, in regulating the MAP kinase pathway and Na+/H+exchange in colonocytes. We demonstrate that Ca2+release, mediated by the ZnR, induces phosphorylation of ERK1/2, which is highly metal-specific, mediated by physiological concentrations of extracellular Zn2+but not by Cd2+, Fe2+, Ni2+, or Mn2+. Desensitization of the ZnR by Zn2+, is followed by ∼90% inhibition of the Zn2+-dependent ERK1/2 phosphorylation, indicating that the ZnR is a principal link between extracellular Zn2+and ERK1/2 activation. Application of both the IP3pathway and PI 3-kinase antagonists largely inhibited Zn2+-dependent ERK1/2 phosphorylation. The physiological significance of the Zn2+-dependent activation of ERK1/2 was addressed by monitoring Na+/H+exchanger activity in HT29 cells and in native colon epithelium. Preincubation of the cells with zinc was followed by robust activation of Na+/H+exchange, which was eliminated by cariporide (0.5 μm); indicating that zinc enhances the activity of NHE1. Activation of NHE1 by zinc was totally blocked by the ERK1/2 inhibitor, U0126. Prolonged acidification, in contrast, stimulates NHE1 by a distinct pathway that is not affected by extracellular Zn2+or inhibitors of the MAP kinase pathway. Desensitization of ZnR activity eliminates the Zn2+-dependent, but not the prolonged acidification-dependent activation of NHE1, indicating that Zn2+-dependent activation of H+extrusion is specifically mediated by the ZnR. Our results support a role for extracellular zinc, acting through the ZnR, in regulating multiple signaling pathways that affect pH homeostasis in colonocytes. Furthermore activation of both, ERK and NHE1, by extracellular zinc may provide the mechanism linking zinc to enhanced cell proliferation.

scholarly journals Poplar bark lipids enhance mouse immunity by inducing T cell proliferation and differentiation

2020 ◽  
Vol 82 (8) ◽  
pp. 1187-1196
Author(s):  
Jinxiu TANG ◽  
Xiuli WEI ◽  
Youzhi LI ◽  
Linlin JIANG ◽  
Tao FENG ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
T Cell Proliferation ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

scholarly journals The protective role of human ghrelin in sepsis: Restoration of CD4 T cell proliferation

PLoS ONE ◽  
2018 ◽  
Vol 13 (7) ◽  
pp. e0201139 ◽  
Author(s):  
Mian Zhou ◽  
Monowar Aziz ◽  
Manhendar Ochani ◽  
Weng-Lang Yang ◽  
Archna Sharma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Protective Role ◽  
Cd4 T Cell ◽  
T Cell Proliferation

T-Cell Proliferation and Differentiation

2019 ◽  
pp. 171-176
Author(s):  
N. Avrion Mitchison ◽  
Arno Müllbacher ◽  
Klaus Eichmann
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
T Cell Proliferation ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation
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