scholarly journals Normalization of regulatory T cells, serum TGF-β1, and LTN after 5-aminolevulinic acid-photodynamic therapy in patients with condyloma acuminate

2017 ◽  
Vol 13 (6) ◽  
pp. 3327-3332 ◽  
Author(s):  
Zhang-Yu Bu ◽  
Xiao-Hong Yu ◽  
Li-Min Wu ◽  
Jian-Bo Zhong ◽  
Ping Yang ◽  
...  
Keyword(s):  
T Cells ◽  
Photodynamic Therapy ◽  
Regulatory T Cells ◽  
Aminolevulinic Acid ◽  
Condyloma Acuminate ◽  
Tgf Β1

TGF-β1-induced regulatory T cells

2015 ◽  
Vol 76 (8) ◽  
pp. 561-564 ◽  
Author(s):  
Eva N. Hadaschik ◽  
Alexander H. Enk
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Tgf Β1

scholarly journals Human Dendritic Cells Produce TGF-β1 under the Influence of Lung Carcinoma Cells and Prime the Differentiation of CD4+CD25+Foxp3+Regulatory T Cells

2009 ◽  
Vol 182 (5) ◽  
pp. 2795-2807 ◽  
Author(s):  
Ingrid E. Dumitriu ◽  
Donald R. Dunbar ◽  
Sarah E. Howie ◽  
Tariq Sethi ◽  
Christopher D. Gregory
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Regulatory T Cells ◽  
Lung Carcinoma ◽  
Carcinoma Cells ◽  
Lung Carcinoma Cells ◽  
Human Dendritic Cells ◽  
Tgf Β1

scholarly journals Absence of signaling into CD4+ cells via C3aR and C5aR enables autoinductive TGF-β1 signaling and induction of Foxp3+ regulatory T cells

2012 ◽  
Vol 14 (2) ◽  
pp. 162-171 ◽  
Author(s):  
Michael G Strainic ◽  
Ethan M Shevach ◽  
Fengqi An ◽  
Feng Lin ◽  
M Edward Medof
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cd4 Cells ◽  
Tgf Β1

scholarly journals Dendritic Cells With TGF-β1 and IL-2 Differentiate Naive CD4+ T Cells Into Alloantigen-Specific and Allograft Protective Foxp3+ Regulatory T Cells

2012 ◽  
Vol 93 (6) ◽  
pp. 580-588 ◽  
Author(s):  
Hua Yang ◽  
Elaine Y. Cheng ◽  
Vijay K. Sharma ◽  
Mila Lagman ◽  
Christina Chang ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Regulatory T Cells ◽  
Cd4 T Cells ◽  
Tgf Β1

scholarly journals Targeting neuropilin-1 suppresses the stability of CD4+CD25+ regulatory T cells via the NF-κB signaling pathway in sepsis

2020 ◽  
Author(s):  
Yu-lei Gao ◽  
Chun-xue Wang ◽  
Zi-yi Wang ◽  
Wen-jie Li ◽  
Yan-cun Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Signaling Pathway ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Sepsis Model ◽  
The Stability ◽  
The Impact ◽  
Tgf Β1

Neuropilin (Nrp)-1 contributes to maintain the stability of CD4+CD25+ regulatory T cells (Tregs). We investigated the impact of Nrp-1 on the stability of CD4+CD25+ Tregs, and the underlying signaling pathways, in a sepsis model. Splenic CD4+CD25+ Tregs were treated with anti-Nrp-1, or transfected to silence Nrp-1 and ikkβ, or administered with PDTC, followed by rSema3A in sepsis simulation. After creation of a sepsis model in mice, anti-Nrp-1 was administered. Expression of foxp3- TSDR, apoptosis rate, Foxp-3/CTLA-4/TGF-β1, IL-10 and TGF-β1, and NF-κB signaling activity of CD4+CD25+ Tregs were determined. Sepsis simulation with or without rSema3A increased the stability of CD4+CD25+ Tregs, including an increase in the expression of Foxp-3/CTLA-4/TGF-β1, decrease in apoptosis and methylation of foxp3- TSDR, increase in the secretion of TGF-β1 and IL-10, and increase in the immunosuppressive effect on CD4+T lymphocytes. silencing of Nrp-1 or anti-Nrp-1 treatment interdicted LPS stimulation with or without a rSema3A-mediated effect. Sepsis simulation increased the DNA-binding activity of NF-κB, as well as the p-ikkβ/ikkβ and p-P65/P65 ratios in vitro and vivo. Silencing of ikkβ expression or PDTC treatment suppressed the stability of CD4+CD25+ Tregs in LPS-induced sepsis. Weakening Nrp-1 reduced the stability of CD4+CD25+ Tregs by regulating the NF-κB signaling pathway, and could be a new target for immunoregulation in sepsis.

scholarly journals Ionizing radiation modulates the phenotype and function of human CD4+ induced regulatory T cells

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Samantha S. Beauford ◽  
Anita Kumari ◽  
Charlie Garnett-Benson
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Tumor Immunity ◽  
Foxp3 Expression ◽  
Cytotoxic T Cell ◽  
Suppressive Activity ◽  
Tgf Β1

Abstract Background The use of immunotherapy strategies for the treatment of advanced cancer is rapidly increasing. Most immunotherapies rely on induction of CD8+ tumor-specific cytotoxic T cells that are capable of directly killing cancer cells. Tumors, however, utilize a variety of mechanisms that can suppress anti-tumor immunity. CD4+ regulatory T cells can directly inhibit cytotoxic T cell activity and these cells can be recruited, or induced, by cancer cells allowing escape from immune attack. The use of ionizing radiation as a treatment for cancer has been shown to enhance anti-tumor immunity by several mechanisms including immunogenic tumor cell death and phenotypic modulation of tumor cells. Less is known about the impact of radiation directly on suppressive regulatory T cells. In this study we investigate the direct effect of radiation on human TREG viability, phenotype, and suppressive activity. Results Both natural and TGF-β1-induced CD4+ TREG cells exhibited increased resistance to radiation (10 Gy) as compared to CD4+ conventional T cells. Treatment, however, decreased Foxp3 expression in natural and induced TREG cells and the reduction was more robust in induced TREGS. Radiation also modulated the expression of signature iTREG molecules, inducing increased expression of LAG-3 and decreased expression of CD25 and CTLA-4. Despite the disconcordant modulation of suppressive molecules, irradiated iTREGS exhibited a reduced capacity to suppress the proliferation of CD8+ T cells. Conclusions Our findings demonstrate that while human TREG cells are more resistant to radiation-induced death, treatment causes downregulation of Foxp3 expression, as well as modulation in the expression of TREG signature molecules associated with suppressive activity. Functionally, irradiated TGF-β1-induced TREGS were less effective at inhibiting CD8+ T cell proliferation. These data suggest that doses of radiotherapy in the hypofractionated range could be utilized to effectively target and reduce TREG activity, particularly when used in combination with cancer immunotherapies.

scholarly journals Cutting Edge: Hypoxia-Induced Nanog Favors the Intratumoral Infiltration of Regulatory T Cells and Macrophages via Direct Regulation of TGF-β1

2013 ◽  
Vol 191 (12) ◽  
pp. 5802-5806 ◽  
Author(s):  
Meriem Hasmim ◽  
Muhammad Zaeem Noman ◽  
Yosra Messai ◽  
Didier Bordereaux ◽  
Gwendoline Gros ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cutting Edge ◽  
Tgf Β1 ◽  
Direct Regulation

scholarly journals GARP Is Regulated by miRNAs and Controls Latent TGF-β1 Production by Human Regulatory T Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e76186 ◽  
Author(s):  
Emilie Gauthy ◽  
Julia Cuende ◽  
Julie Stockis ◽  
Caroline Huygens ◽  
Bernard Lethé ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Tgf Β1

CD28 disruption exacerbates inflammation in Tgf-β1-/- mice: in vivo suppression by CD4+CD25+ regulatory T cells independent of autocrine TGF-β1

Blood ◽  
2004 ◽  
Vol 103 (12) ◽  
pp. 4594-4601 ◽  
Author(s):  
Mizuko Mamura ◽  
WoonKyu Lee ◽  
Timothy J. Sullivan ◽  
Angelina Felici ◽  
Anastasia L. Sowers ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Transforming Growth Factor ◽  
Cytotoxic T Lymphocyte ◽  
Tumor Necrosis Factor Receptor ◽  
Transforming Growth Factor Β1 ◽  
Autoimmune Inflammatory Disease ◽  
Lymph Node Cells ◽  
Tgf Β1

Abstract Tgf-β1-/- mice develop a progressive, lethal, inflammatory syndrome, but mechanisms leading to the spontaneous activation of Tgf-β1-/- T cells remain unclear. Here we show the disruption of CD28 gene expression accelerates disease in Tgf-β1-/- mice, and we link this increase in severity to a reduction in the number of CD4+CD25+ regulatory T cells. CD4+CD25+ T cells develop normally in Tgf-β1-/- mice and display characteristic expression of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), glucocorticoid-induced tumor necrosis factor receptor (GITR), αEβ7 integrin, and Foxp3. Adoptive transfer of Tgf-β1-/- splenocytes to Tgf-β1+/+/Rag2-/- mice induced an autoimmune inflammatory disease with features similar to those of the Tgf-β1-/- phenotype, and disease transfer was accelerated by the depletion of Tgf-β1-/- CD4+CD25+ T cells from donor splenocytes. Cotransfer of Tgf- β1-/- CD4+CD25+ T cells clearly attenuated disease in Rag2-/- recipients of CD25+-depleted Tgf-β1-/- spleen and lymph node cells, but suppression was incomplete when compared with Tgf-β1+/+ CD4+CD25+ T cells. These data demonstrate that CD4+CD25+ regulatory T cells develop in complete absence of endogenous transforming growth factor-β1 (TGF-β1) expression and that autocrine TGF-β1 expression is not essential for these cells to suppress inflammation in vivo. (Blood. 2004;103:4594-4601)

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