scholarly journals Post‐transcriptional control of T cell cytokine production: implications for cancer therapy

Immunology ◽  
2021 ◽  
Author(s):  
Julian J. Freen‐van Heeren
Keyword(s):  
T Cell ◽  
Cancer Therapy ◽  
Transcriptional Control ◽  
Cytokine Production ◽  
Cell Cytokine Production

Modulation of T cell cytokine production by miR-144* with elevated expression in patients with pulmonary tuberculosis

2011 ◽  
Vol 48 (9-10) ◽  
pp. 1084-1090 ◽  
Author(s):  
Yanhua Liu ◽  
Xinjing Wang ◽  
Jing Jiang ◽  
Zhihong Cao ◽  
Bingfen Yang ◽  
...  
Keyword(s):  
T Cell ◽  
Pulmonary Tuberculosis ◽  
Cytokine Production ◽  
Elevated Expression ◽  
Cell Cytokine Production

The Role of Accessory Cell Products in the Regulation of T Cell Cytokine Production

1996 ◽  
pp. 305-308 ◽  
Author(s):  
M. L. Kapsenberg ◽  
C. M. U. Hilkens ◽  
T. C. T. M. Pouw van der Kraan ◽  
E. A. Wierenga ◽  
A. Snijders
Keyword(s):  
T Cell ◽  
Cytokine Production ◽  
Accessory Cell ◽  
Cell Cytokine Production

scholarly journals T Cell Tolerance Induced by Cross-Reactive TCR Ligands Can Be Broken by Superagonist Resulting in Anti-Inflammatory T Cell Cytokine Production

2005 ◽  
Vol 175 (3) ◽  
pp. 1491-1497 ◽  
Author(s):  
Zsolt Illés ◽  
Hanspeter Waldner ◽  
Jayagopala Reddy ◽  
Estelle Bettelli ◽  
Lindsay B. Nicholson ◽  
...  
Keyword(s):  
T Cell ◽  
Cytokine Production ◽  
T Cell Tolerance ◽  
Cell Tolerance ◽  
Anti Inflammatory ◽  
Cell Cytokine Production

Salutary effects of 17β-estradiol on T-cell signaling and cytokine production after trauma-hemorrhage are mediated primarily via estrogen receptor-α

2007 ◽  
Vol 292 (6) ◽  
pp. C2103-C2111 ◽  
Author(s):  
Takao Suzuki ◽  
Tomoharu Shimizu ◽  
Huang-Ping Yu ◽  
Ya-Ching Hsieh ◽  
Mashkoor A. Choudhry ◽  
...  
Keyword(s):  
T Cells ◽  
Estrogen Receptor ◽  
T Cell ◽  
Signaling Pathways ◽  
Cytokine Production ◽  
Estrogen Receptor Α ◽  
Male Rats ◽  
17Β Estradiol ◽  
Ifn Γ ◽  
Cell Cytokine Production

Although 17β-estradiol (E2) administration following trauma-hemorrhage prevents the suppression in splenocyte cytokine production, it remains unknown whether the salutary effects of 17β-estradiol are mediated via estrogen receptor (ER)-α or ER-β. Moreover, it is unknown which signaling pathways are involved in 17β-estradiol's salutary effects. Utilizing an ER-α- or ER-β-specific agonist, we examined the role of ER-α and ER-β in E2-mediated restoration of T-cell cytokine production following trauma-hemorrhage. Moreover, since MAPK, NF-κB, and activator protein (AP)-1 are known to regulate T-cell cytokine production, we also examined the activation of MAPK, NF-κB, and AP-1. Male rats underwent trauma-hemorrhage (mean arterial pressure 40 mmHg for 90 min) and fluid resuscitation. ER-α agonist propyl pyrazole triol (PPT; 5 μg/kg), ER-β agonist diarylpropionitrile (DPN; 5 μg/kg), 17β-estradiol (50 μg/kg), or vehicle (10% DMSO) was injected subcutaneously during resuscitation. Twenty-four hours thereafter, splenic T cells were isolated, and their IL-2 and IFN-γ production and MAPK, NF-κB, and AP-1 activation were measured. T-cell IL-2 and IFN-γ production was decreased following trauma-hemorrhage, and this was accompanied with a decrease in T-cell MAPK, NF-κB, and AP-1 activation. PPT or 17β-estradiol administration following trauma-hemorrhage normalized those parameters, while DPN administration had no effect. Since PPT, but not DPN, administration following trauma-hemorrhage was as effective as 17β-estradiol in preventing the T-cell suppression, it appears that ER-α plays a predominant role in mediating the salutary effects of 17β-estradiol on T cells following trauma-hemorrhage, and that such effects are likely mediated via normalization of MAPK, NF-κB, and AP-1 signaling pathways.

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