Newly discovered role for Fas ligand in the cell-cycle arrest of CD4+ T cells

10.1038/3965 ◽  
1998 ◽  
Vol 4 (12) ◽  
pp. 1377-1382 ◽  
Author(s):  
Julie Desbarats ◽  
Richard C. Duke ◽  
M. Karen Newell
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cell Cycle Arrest ◽  
Cd4 T Cells ◽  
Fas Ligand ◽  
Cycle Arrest

scholarly journals Semi-purified extracts of Commelina benghalensis (Commelinaceae) induce apoptosis and cell cycle arrest in Jurkat-T cells

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Kgomotso Welheminah Lebogo ◽  
Matlou Phineas Mokgotho ◽  
Victor Patrick Bagla ◽  
Thabe Moses Matsebatlela ◽  
Vusi Mbazima ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cell Cycle Arrest ◽  
Jurkat T Cells ◽  
Commelina Benghalensis ◽  
Cycle Arrest

scholarly journals Vasoactive Intestinal Peptide Induces Cell Cycle Arrest and Regulatory Functions in Human T Cells at Multiple Levels

2010 ◽  
Vol 30 (10) ◽  
pp. 2537-2551 ◽  
Author(s):  
Per Anderson ◽  
Elena Gonzalez-Rey
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cell Cycle Arrest ◽  
Vasoactive Intestinal Peptide ◽  
Molecular Mechanisms ◽  
Cytotoxic T Lymphocyte ◽  
Interleukin 2 ◽  
Experimental Models ◽  
Cycle Arrest ◽  
Human T Cells

ABSTRACT Vasoactive intestinal peptide (VIP) is a potent anti-inflammatory neuropeptide that, by inhibiting Th1-driven responses and inducing the emergence of regulatory T cells (Treg), has been proven successful in the induction of tolerance in various experimental models of autoimmune disorders. Here, we investigate the molecular mechanisms involved in VIP-induced tolerance. VIP treatment in the presence of T-cell receptor (TCR) signaling and CD28 costimulation induced cell cycle arrest in human T cells. VIP blocked G1/S transition and inhibited the synthesis of cyclins D3 and E and the activation of the cyclin-dependent kinases (CDKs) cdk2 and cdk4. This effect was accompanied by maintenance of threshold levels of the CDK inhibitor p27kip1 and impairment of phosphatidylinositol 3-kinase (PI3K)-Akt signaling. Inhibition of interleukin 2 (IL-2) transcription and downregulation of signaling through NFAT, AP-1, and Ras-Raf paralleled the VIP-induced cell cycle arrest. Noteworthy from a functional point of view is the fact that VIP-treated T cells show a regulatory phenotype characterized by high expression of CD25, cytotoxic-T-lymphocyte-associated protein 4 (CTLA4), and Forkhead box protein 3 (FoxP3) and potent suppressive activities against effector T cells. CTLA4 appears to be critically involved in the generation and suppressive activities of VIP-induced Treg. Finally, cyclic AMP (cAMP) and protein kinase A (PKA) activation seems to mediate the VIP-induced cell cycle arrest and Treg generation.

A Secreted Low--Molecular-Weight Protein From Helicobacter pylori Induces Cell-Cycle Arrest of T Cells

2005 ◽  
Vol 128 (5) ◽  
pp. 1327-1339 ◽  
Author(s):  
Markus Gerhard ◽  
Christian Schmees ◽  
Petra Voland ◽  
Nicole Endres ◽  
Markus Sander ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Molecular Weight ◽  
T Cells ◽  
Helicobacter Pylori ◽  
Cell Cycle Arrest ◽  
Low Molecular Weight ◽  
Molecular Weight Protein ◽  
Cycle Arrest ◽  
Weight Protein ◽  
Low Molecular Weight Protein

scholarly journals Protein Kinase A Phosphorylation Activates Vpr-Induced Cell Cycle Arrest during Human Immunodeficiency Virus Type 1 Infection

2010 ◽  
Vol 84 (13) ◽  
pp. 6410-6424 ◽  
Author(s):  
R. Anthony Barnitz ◽  
Fengyi Wan ◽  
Vinay Tripuraneni ◽  
Diane L. Bolton ◽  
Michael J. Lenardo
Keyword(s):  
Cell Cycle ◽  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Protein Kinase ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Kinase A

ABSTRACT Infection with human immunodeficiency virus type 1 (HIV-1) causes an inexorable depletion of CD4+ T cells. The loss of these cells is particularly pronounced in the mucosal immune system during acute infection, and the data suggest that direct viral cytopathicity is a major factor. Cell cycle arrest caused by the HIV-1 accessory protein Vpr is strongly correlated with virus-induced cell death, and phosphorylation of Vpr serine 79 (S79) is required to activate G2/M cell cycle blockade. However, the kinase responsible for phosphorylating Vpr remains unknown. Our bioinformatic analyses revealed that S79 is part of a putative phosphorylation site recognized by protein kinase A (PKA). We show here that PKA interacts with Vpr and directly phosphorylates S79. Inhibition of PKA activity during HIV-1 infection abrogates Vpr cell cycle arrest. These findings provide new insight into the signaling event that activates Vpr cell cycle arrest, ultimately leading to the death of infected T cells.

The Hsp40 family chaperone protein DnaJB6 enhances Schlafen1 nuclear localization which is critical for promotion of cell-cycle arrest in T-cells

2008 ◽  
Vol 413 (2) ◽  
pp. 239-250 ◽  
Author(s):  
Yafeng Zhang ◽  
Zhengmin Yang ◽  
Yonghao Cao ◽  
Shijian Zhang ◽  
Hai Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
T Cell ◽  
T Lymphocytes ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Nuclear Localization ◽  
Nuclear Import ◽  
Cycle Arrest ◽  
Chaperone Protein

Tight control of cell-cycle progression is critical for T-lymphocytes to function properly. Slfn1 (Schlafen1) has been reported to play an important role in the establishment and maintenance of quiescence in T-lymphocytes. However, how Slfn1 accomplishes this critical function remains poorly understood. In the present study, we show that nuclear localization is a prerequisite for Slfn1 to induce cell-cycle arrest, with DnaJB6, identified as a new Slfn1-binding protein, playing a pivotal role in this process. DnaJB6, a chaperone protein of the DnaJ/Hsp (heat-shock protein) 40 family, stabilizes Slfn1 together with its partner Hsp70, and, more importantly, it enhances the nuclear import of Slfn1. Overexpression of DnaJB6 was found to increase Slfn1 nuclear accumulation and resulted in cell-cycle arrest, whereas, in DnaJB6 knock-down cells, Slfn1 was mainly sequestered in the cytoplasm and no cell-cycle arrest was observed. Furthermore, transgenic expression of DnaJB6 in T-lineage cells inhibited Slfn1's degradation, promoted its nuclear import and ultimately led to suppression of T-cell proliferation upon TCR (T-cell receptor) activation. In addition, DnaJB6 increased Slfn1's effect on its downstream target cyclin D1 in co-transfected cells. Altogether, our results demonstrate that DnaJB6 is necessary for translocation of Slfn1 into the nucleus, where Slfn1 down-regulates cyclin D1, induces cell-cycle arrest and programmes a quiescent state of T-cells.

Mesenchymal stem cell-derived exosomes suppress proliferation of T cells by inducing cell cycle arrest through p27kip1/Cdk2 signaling

2020 ◽  
Vol 225 ◽  
pp. 16-22 ◽  
Author(s):  
Sunho Lee ◽  
Sueon Kim ◽  
Hyunwoo Chung ◽  
Ji Hwan Moon ◽  
Seong Jun Kang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cell Cycle Arrest ◽  
Cycle Arrest

scholarly journals G1/S cell cycle arrest provoked in human T cells by antibody to CD26

Immunology ◽  
2002 ◽  
Vol 107 (3) ◽  
pp. 325-333 ◽  
Author(s):  
Kei Ohnuma ◽  
Tomonori Ishii ◽  
Satoshi Iwata ◽  
Osamu Hosono ◽  
Hiroshi Kawasaki ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Human T Cells
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