scholarly journals Transforming growth factor-  inhibits human antigen-specific CD4+ T cell proliferation without modulating the cytokine response

2003 ◽  
Vol 15 (12) ◽  
pp. 1495-1504 ◽  
Author(s):  
M. M. Tiemessen
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Cytokine Response ◽  
Cd4 T Cell ◽  
T Cell Proliferation

scholarly journals Latency-Associated Peptide of Transforming Growth Factor β Enhances Mycobacteriocidal Immunity in the Lung duringMycobacterium bovis BCG Infection in C57BL/6 Mice

2000 ◽  
Vol 68 (11) ◽  
pp. 6505-6508 ◽  
Author(s):  
K. A. Wilkinson ◽  
T. D. Martin ◽  
S. M. Reba ◽  
H. Aung ◽  
R. W. Redline ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Growth Factor ◽  
Mrna Expression ◽  
Mycobacterium Bovis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Gamma Interferon ◽  
T Cell Proliferation

ABSTRACT Latency-associated peptide of transforming growth factor β (TGF-β) (LAP) was used to determine whether in vivo modulation of TGF-β bioactivity enhanced pulmonary immunity to Mycobacterium bovis BCG infection in C57BL/6 mice. LAP decreased BCG growth in the lung and enhanced antigen-specific T-cell proliferation and gamma interferon mRNA expression. Thus, susceptibility of the lung to primary BCG infection may be partially mediated by the immunosuppressive effects of TGF-β.

scholarly journals Defective T-Cell Activation Is Associated with Augmented Transforming Growth Factor β Sensitivity in Mice with Mutations in the Sno Gene

2003 ◽  
Vol 23 (15) ◽  
pp. 5446-5459 ◽  
Author(s):  
S. Pearson-White ◽  
M. McDuffie
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Negative Regulator ◽  
Mutant Mice ◽  
T Cell Proliferation ◽  
Receptor Ligation

ABSTRACT The proto-oncogene Sno has been shown to be a negative regulator of transforming growth factor beta (TGF-β) signaling in vitro, using overexpression and artificial reporter systems. To examine Sno function in vivo, we made two targeted deletions at the Sno locus: a 5′ deletion, with reduced Sno protein (hypomorph), and an exon 1 deletion removing half the protein coding sequence, in which Sno protein is undetectable in homozygotes (null). Homozygous Sno hypomorph and null mutant mice are viable without gross developmental defects. We found that Sno mRNA is constitutively expressed in normal thymocytes and splenic T cells, with increased expression 1 h following T-cell receptor ligation. Although thymocyte and splenic T-cell populations appeared normal in mutant mice, T-cell proliferation in response to activating stimuli was defective in both mutant strains. This defect could be reversed by incubation with either anti-TGF-β antibodies or exogenous interleukin-2 (IL-2). Together, these findings suggest that Sno-dependent suppression of TGF-β signaling is required for upregulation of growth factor production and normal T-cell proliferation following receptor ligation. Indeed, both IL-2 and IL-4 levels are reduced in response to anti-CD3ε stimulation of mutant T cells, and transfected Sno activated an IL-2 reporter system in non-T cells. Mutant mouse embryo fibroblasts also exhibited a reduced cell proliferation rate that could be reversed by administration of anti-TGF-β. Our data provide strong evidence that Sno is a significant negative regulator of antiproliferative TGF-β signaling in both T cells and other cell types in vivo.

scholarly journals IL-12–Dependent Cytomegalovirus-Specific CD4+T Cell Proliferation, T-bet Induction, and Effector Multifunction during Primary Infection Are Key Determinants for Early Immune Control

2015 ◽  
Vol 196 (2) ◽  
pp. 877-890 ◽  
Author(s):  
Iulia Popescu ◽  
Matthew R. Pipeling ◽  
Hannah Mannem ◽  
Pali D. Shah ◽  
Jonathan B. Orens ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Primary Infection ◽  
Cd4 T Cell ◽  
T Cell Proliferation ◽  
Immune Control

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.

scholarly journals Adenosine produced by a CD38-mediated pathway in CD56bright CD16- NK cells inhibits autologous CD4+T cell proliferation

2013 ◽  
Vol 4 ◽  
Author(s):  
Morandi Fabio ◽  
Horenstein Alberto ◽  
Chillemi Antonella ◽  
Zaccarello Gianluca ◽  
Malavasi Fabio ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Nk Cells ◽  
Cd4 T Cell ◽  
T Cell Proliferation
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