scholarly journals Tolerogenic Dendritic Cells Induce CD4+CD25hiFoxp3+ Regulatory T Cell Differentiation from CD4+CD25−/loFoxp3− Effector T Cells

2010 ◽  
Vol 185 (9) ◽  
pp. 5003-5010 ◽  
Author(s):  
Hui Huang ◽  
Wojciech Dawicki ◽  
Xiaobei Zhang ◽  
Jennifer Town ◽  
John R. Gordon
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Regulatory T Cell ◽  
Effector T Cells ◽  
T Cell Differentiation ◽  
Tolerogenic Dendritic Cells

scholarly journals Midkine Inhibits Inducible Regulatory T Cell Differentiation by Suppressing the Development of Tolerogenic Dendritic Cells

2012 ◽  
Vol 188 (6) ◽  
pp. 2602-2611 ◽  
Author(s):  
Yoshifumi Sonobe ◽  
Hua Li ◽  
Shijie Jin ◽  
Satoshi Kishida ◽  
Kenji Kadomatsu ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Regulatory T Cell ◽  
T Cell Differentiation ◽  
Tolerogenic Dendritic Cells

scholarly journals HTLV-1 induces T cell malignancy and inflammation by viral antisense factor-mediated modulation of the cytokine signaling

2020 ◽  
Vol 117 (24) ◽  
pp. 13740-13749 ◽  
Author(s):  
Yusuke Higuchi ◽  
Jun-ichirou Yasunaga ◽  
Yu Mitagami ◽  
Hirotake Tsukamoto ◽  
Kazutaka Nakashima ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Transgenic Mice ◽  
Regulatory T Cell ◽  
T Cell Differentiation ◽  
Cytokine Signaling ◽  
Viral Gene ◽  
Cell Leukemia Virus Type ◽  
Human T Cell

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of a T cell neoplasm and several inflammatory diseases. A viral gene, HTLV-1 bZIP factor (HBZ), induces pathogenic Foxp3-expressing T cells and triggers systemic inflammation and T cell lymphoma in transgenic mice, indicating its significance in HTLV-1–associated diseases. Here we show that, unexpectedly, a proinflammatory cytokine, IL-6, counteracts HBZ-mediated pathogenesis. Loss of IL-6 accelerates inflammation and lymphomagenesis in HBZ transgenic mice. IL-6 innately inhibits regulatory T cell differentiation, suggesting that IL-6 functions as a suppressor against HBZ-associated complications. HBZ up-regulates expression of the immunosuppressive cytokine IL-10. IL-10 promotes T cell proliferation only in the presence of HBZ. As a mechanism of growth promotion by IL-10, HBZ interacts with STAT1 and STAT3 and modulates the IL-10/JAK/STAT signaling pathway. These findings suggest that HTLV-1 promotes the proliferation of infected T cells by hijacking the machinery of regulatory T cell differentiation. IL-10 induced by HBZ likely suppresses the host immune response and concurrently promotes the proliferation of HTLV-1 infected T cells.

Generation and biochemical analysis of human effector CD4 T cells: alterations in tyrosine phosphorylation and loss of CD3ζ expression

Blood ◽  
2001 ◽  
Vol 97 (12) ◽  
pp. 3851-3859 ◽  
Author(s):  
Sandeep Krishnan ◽  
Vishal G. Warke ◽  
Madhusoodana P. Nambiar ◽  
Henry K. Wong ◽  
George C. Tsokos ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Tyrosine Phosphorylation ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Effector T Cells ◽  
T Cell Differentiation ◽  
Effector T Cell

Human effector T cells have been difficult to isolate and characterize due to their phenotypic and functional similarity to the memory subset. In this study, a biochemical approach was used to analyze human effector CD4 T cells generated in vitro by activation with anti-CD3 and autologous monocytes for 3 to 5 days. The resultant effector cells expressed the appropriate activation/differentiation markers and secreted high levels of interferon γ (IFN-γ) when restimulated. Biochemically, effector CD4 T cells exhibited increases in total intracellular tyrosine phosphorylation and effector-associated phosphorylated species. Paradoxically, these alterations in tyrosine phosphorylation were concomitant with greatly reduced expression of CD3ζ and CD3ε signaling subunits coincident with a reduction in surface T-cell receptor (TCR) expression. Because loss of CD3ζ has also been detected in T cells isolated ex vivo from individuals with cancer, chronic viral infection, and autoimmune diseases, the requirements and kinetics of CD3ζ down-regulation were examined. The loss of CD3ζ expression persisted throughout the course of effector T-cell differentiation, was reversible on removal from the activating stimulus, and was modulated by activation conditions. These biochemical changes occurred in effector T cells generated from naive or memory CD4 T-cell precursors and distinguished effector from memory T cells. The results suggest that human effector T-cell differentiation is accompanied by alterations in the TCR signal transduction and that loss of CD3ζ expression may be a feature of chronic T-cell activation and effector generation in vivo.

scholarly journals Effector T Cells Boost Regulatory T Cell Expansion by IL-2, TNF, OX40, and Plasmacytoid Dendritic Cells Depending on the Immune Context

2014 ◽  
Vol 194 (3) ◽  
pp. 999-1010 ◽  
Author(s):  
Audrey Baeyens ◽  
David Saadoun ◽  
Fabienne Billiard ◽  
Angéline Rouers ◽  
Sylvie Grégoire ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Regulatory T Cell ◽  
Cell Expansion ◽  
Plasmacytoid Dendritic Cells ◽  
Effector T Cells ◽  
T Cell Expansion

scholarly journals Dendritic cells treated with a prostaglandin I2 analog, iloprost, promote antigen-specific regulatory T cell differentiation in mice

2020 ◽  
Vol 79 ◽  
pp. 106106 ◽  
Author(s):  
Tzu-Hsuan Wong ◽  
Rung-Jiun Gau ◽  
Yu-Fang Chen ◽  
Hsin-Hsin Shen ◽  
Carl Tsai-Yu Lin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Regulatory T Cell ◽  
T Cell Differentiation ◽  
Prostaglandin I2
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