scholarly journals Programmed Death-1 Inhibition of Phosphatidylinositol 3-Kinase/AKT/Mechanistic Target of Rapamycin Signaling Impairs Sarcoidosis CD4+T Cell Proliferation

2017 ◽  
Vol 56 (1) ◽  
pp. 74-82 ◽  
Author(s):  
Lindsay J. Celada ◽  
Joseph E. Rotsinger ◽  
Anjuli Young ◽  
Guzel Shaginurova ◽  
Debresha Shelton ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Cd4 T Cell ◽  
Target Of Rapamycin ◽  
T Cell Proliferation ◽  
Phosphatidylinositol 3 Kinase ◽  
Mechanistic Target Of Rapamycin ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Phosphatidylinositol 3

scholarly journals Naive CD4 T Cell Proliferation Is Controlled by Mammalian Target of Rapamycin Regulation of GRAIL Expression

2009 ◽  
Vol 182 (10) ◽  
pp. 5919-5928 ◽  
Author(s):  
Jack T. Lin ◽  
Neil B. Lineberry ◽  
Michael G. Kattah ◽  
Leon L. Su ◽  
Paul J. Utz ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Mammalian Target Of Rapamycin ◽  
Cd4 T Cell ◽  
Target Of Rapamycin ◽  
T Cell Proliferation

212 Programmed death-1 pathway inhibit γ-common cytokines signal–driven T-cell Proliferation and Survival

Cytokine ◽  
2008 ◽  
Vol 43 (3) ◽  
pp. 289-290
Author(s):  
Wei Huang ◽  
Andre Tanel ◽  
Francesco A Procopio ◽  
Simmone Fonseca ◽  
Bader Yassine-Diab ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
T Cell Proliferation ◽  
Programmed Death ◽  
Programmed Death 1

scholarly journals A Late, Prolonged Activation of the Phosphatidylinositol 3-Kinase Pathway Is Required for T Cell Proliferation

2004 ◽  
Vol 172 (6) ◽  
pp. 3527-3534 ◽  
Author(s):  
Ferdinand V. Lali ◽  
James Crawley ◽  
Derek A. McCulloch ◽  
Brian M. J. Foxwell
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
T Cell Proliferation ◽  
Phosphatidylinositol 3 Kinase ◽  
Kinase Pathway ◽  
Phosphatidylinositol 3

scholarly journals Impaired Induction of CD27 and CD28 Predicts Naive CD4 T Cell Proliferation Defects in HIV Disease

2007 ◽  
Vol 179 (6) ◽  
pp. 3543-3549 ◽  
Author(s):  
Angel A. Luciano ◽  
Michael M. Lederman ◽  
Alice Valentin-Torres ◽  
Douglas A. Bazdar ◽  
Scott F. Sieg
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Cd4 T Cell ◽  
T Cell Proliferation ◽  
Hiv Disease

scholarly journals Miquelianin Inhibits Allergic Responses in Mice by Suppressing CD4+ T Cell Proliferation

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1120
Author(s):  
Dae Woon Choi ◽  
Sun Young Jung ◽  
Gun-Dong Kim ◽  
So-Young Lee ◽  
Hee Soon Shin
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Mouse Model ◽  
Immune Responses ◽  
Reactive Oxygen Species Generation ◽  
Allergic Diseases ◽  
Cd4 T Cell ◽  
Th2 Cells ◽  
T Cell Proliferation ◽  
Heme Oxygenase 1

Allergic diseases, including atopic dermatitis (AD), induce type 2 helper T (Th2) cell-dominant immune responses. Miquelianin (quercetin 3-O-glucuronide, MQL) is an active compound in Rosae multiflorae fructus extract with anti-allergic properties. Here, we investigate the anti-allergic effects of MQL in an ovalbumin (OVA)-induced Th2-dominant mouse model and the associated mechanisms. Oral MQL suppressed cytokine and IL-2 production and proliferation of Th2 cells and upregulated heme oxygenase-1 (HO-1) in splenocytes. Ex vivo MQL suppressed Th1- and Th2-related immune responses by inhibiting CD4+ T cell proliferation, and upregulated HO-1 in CD4+ T cells by activating C-Raf–ERK1/2–Nrf2 pathway via induction of reactive oxygen species generation. In a trimellitic anhydride-induced AD-like mouse model, both topical and oral MQL ameliorated AD symptoms by suppressing Th2 immune responses. Our results suggest that MQL is a potential therapeutic agent for CD4+ T cell-mediated diseases, including allergic diseases.

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