Chemical constituents from the fruits of Ligustrum japonicum and their inhibitory effects on T cell activation

2017 ◽  
Vol 141 ◽  
pp. 147-155 ◽  
Author(s):  
Quynh-Mai Thi Ngo ◽  
Hyun-Su Lee ◽  
Van Thu Nguyen ◽  
Jeong Ah Kim ◽  
Mi Hee Woo ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Chemical Constituents ◽  
Inhibitory Effects ◽  
Ligustrum Japonicum

Cyclooxygenase-independent inhibitory effects on T cell activation of novel 4,5-dihydro-3 trifluoromethyl pyrazole cyclooxygenase-2 inhibitors

2010 ◽  
Vol 10 (10) ◽  
pp. 1295-1304 ◽  
Author(s):  
Miguel A. Iñiguez ◽  
Carmen Punzón ◽  
Cristina Cacheiro-Llaguno ◽  
Manuel D. Díaz-Muñoz ◽  
Javier Duque ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cyclooxygenase 2 ◽  
Inhibitory Effects ◽  
Cyclooxygenase 2 Inhibitors

scholarly journals Cutting Edge: Inhibitory Effects of CD4 and CD8 on T Cell Activation Induced by High-Affinity Noncognate Ligands

2009 ◽  
Vol 183 (12) ◽  
pp. 7639-7643 ◽  
Author(s):  
Adam S. Chervin ◽  
Jennifer D. Stone ◽  
Natalie A. Bowerman ◽  
David M. Kranz
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cutting Edge ◽  
Inhibitory Effects ◽  
High Affinity

scholarly journals Prostaglandin E2 and other cyclic AMP elevating agents inhibit interleukin 2 gene transcription by counteracting calcineurin-dependent pathways.

1993 ◽  
Vol 178 (5) ◽  
pp. 1813-1817 ◽  
Author(s):  
F Paliogianni ◽  
R L Kincaid ◽  
D T Boumpas
Keyword(s):  
Signal Transduction ◽  
T Cell ◽  
Prostaglandin E2 ◽  
Gene Transcription ◽  
T Cell Activation ◽  
Promoter Activity ◽  
Cell Activation ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Inhibitory Effects

We have previously shown that prostaglandin E2 and other cAMP elevating agents inhibit the nuclear transcription of the human IL-2 gene by interfering with a Ca(2+)-sensitive T cell signal transduction pathway. Calcineurin, a Ca2+/calmodulin-dependent 2B protein phosphatase, is an essential component of the T cell receptor signal transduction pathway leading to IL-2 gene expression. We have therefore tested the hypothesis that this phosphatase may be a target for the inhibitory effects of cAMP on IL-2 gene transcription. We report here that PGE2 markedly reduces the IL-2 promoter activity that is induced by a constitutively active form of calcineurin. In contrast to the complete inhibition of promoter activity produced by the immunosuppressants cyclosporin A and FK-506, this partial block suggests that PGE2 modulates downstream events needed for lymphokine gene activation. Overexpression of calcineurin in Jurkat cells decreases their apparent sensitivity to the inhibitory effects of PGE2 consistent with the fact that this enzyme plays a physiological role in dephosphorylating substrates of cAMP-dependent kinases in several tissues. These results provide evidence that cAMP-dependent pathways may antagonize calcineurin-regulated cascades for T cell activation in vivo, and suggest crosstalk between the Ca2+ and the cAMP signaling pathways during T cell activation.

scholarly journals SEA Antagonizes the Imatinib-Meditated Inhibitory Effects on T Cell Activation via the TCR Signaling Pathway

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Guanming Wang ◽  
Yuhui Yan ◽  
Xiaohua Chen ◽  
Chen Lin ◽  
Yangqiu Li
Keyword(s):  
T Cells ◽  
T Cell ◽  
Signaling Pathway ◽  
T Cell Activation ◽  
Cell Activation ◽  
Jurkat Cells ◽  
Imatinib Treatment ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Tcr Signaling

The BCR-ABL kinase inhibitor imatinib is highly effective in the treatment of chronic myeloid leukemia (CML). However, long-term imatinib treatment induces immunosuppression, which is mainly due to T cell dysfunction. Imatinib can reduce TCR-triggered T cell activation by inhibiting the phosphorylation of tyrosine kinases such as Lck, ZAP70, LAT, and PLCγ1 early in the TCR signaling pathway. The purpose of this study was to investigate whether the superantigen SEA, a potent T cell stimulator, can block the immunosuppressive effects of imatinib on T cells. Our data show that the exposure of primary human T cells and Jurkat cells to SEA for 24 h leads to the upregulation of the Lck and ZAP70 proteins in a dose-dependent manner. T cells treated with SEA prior to TCR binding had increased the tyrosine phosphorylation of Lck, ZAP70, and PLCγ1. Pretreatment with SEA prevents the inhibitory effects of imatinib on TCR signaling, which leads to T cell proliferation and IL-2 production. It is conceivable that SEA antagonizes the imatinib-mediated inhibition of T cell activation and proliferation through the TCR signaling pathway.

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