scholarly journals Soluble HLA-G Inhibits Cell Cycle Progression in Human Alloreactive T Lymphocytes

2006 ◽  
Vol 176 (3) ◽  
pp. 1331-1339 ◽  
Author(s):  
Rajia Bahri ◽  
Francois Hirsch ◽  
Adeline Josse ◽  
Nathalie Rouas-Freiss ◽  
Nicolas Bidere ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Lymphocytes ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Soluble Hla

SOLUBLE HLA-G INHIBITS CELL CYCLE PROGRESSION IN HUMAN ALLOREACTIVE T LYMPHOCYTES

2004 ◽  
Vol 78 ◽  
pp. 726
Author(s):  
R Bahri ◽  
A Josse ◽  
N Rouas-Freiss ◽  
E D. Carosella ◽  
B Charpentier ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Lymphocytes ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Soluble Hla

scholarly journals Sonic Hedgehog Promotes Cell Cycle Progression in Activated Peripheral CD4+ T Lymphocytes

2002 ◽  
Vol 169 (4) ◽  
pp. 1869-1875 ◽  
Author(s):  
Jacqueline A. Lowrey ◽  
Gareth A. Stewart ◽  
Susannah Lindey ◽  
Gerard F. Hoyne ◽  
Margaret J. Dallman ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Lymphocytes ◽  
Sonic Hedgehog ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Effects of Guanine Nucleotide Depletion on Cell Cycle Progression in Human T Lymphocytes

Blood ◽  
1998 ◽  
Vol 91 (8) ◽  
pp. 2896-2904 ◽  
Author(s):  
Josée Laliberté ◽  
Ann Yee ◽  
Yue Xiong ◽  
Beverly S. Mitchell
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
T Lymphocytes ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Guanine Nucleotides ◽  
Erythroid Cell ◽  
Guanine Nucleotide ◽  
Cycle Progression ◽  
Human T Lymphocytes

Depletion of guanine nucleotide pools after inhibition of inosine monophosphate dehydrogenase (IMPDH) potently inhibits DNA synthesis by arresting cells in G1 and has been shown to induce the differentiation of cultured myeloid and erythroid cell lines, as well as chronic granulocytic leukemic cells after blast transformation. Inhibitors of IMPDH are also highly effective as immunosuppressive agents. The mechanism underlying these pleiotropic effects of depletion of guanine nucleotides is unknown. We have examined the effects of mycophenolic acid (MPA), a potent IMPDH inhibitor, on the cell cycle progression of activated normal human T lymphocytes. MPA treatment resulted in the inhibition of pRb phosphorylation and cell entry into S phase. The expression of cyclin D3, a major component of the cyclin-dependent kinase (CDK) activity required for pRb phosphorylation, was completely abrogated by MPA treatment of T cells activated by interleukin-2 (IL-2) and leucoagglutinin (PHA-L), whereas the expression of cyclin D2, CDK6, and CDK4 was more mildly attenuated. The direct kinase activity of a complex immunoprecipitated with anti-CDK6 antibody was also inhibited. In addition, MPA prevented the IL-2–induced elimination of p27Kip1, a CDK inhibitor, and resulted in the retention of high levels of p27Kip1 in IL-2/PHA-L–treated T cells bound to CDK2. These results indicate that inhibition of the de novo synthesis of guanine nucleotides blocks the transition of normal peripheral blood T lymphocytes from G0 to S phase in early- to mid-G1 and that this cell cycle arrest results from inhibition of the induction of cyclin D/CDK6 kinase and the elimination of p27Kip1 inhibitory activity.

Definition of the Roles for Iron and Essential Fatty Acids in Cell Cycle Progression of Normal Human T Lymphocytes

1993 ◽  
Vol 204 (2) ◽  
pp. 260-267 ◽  
Author(s):  
Naohiro Terada ◽  
Reuven Or ◽  
Agota Szepesi ◽  
Joseph J. Lucas ◽  
Erwin W. Gelfand
Keyword(s):  
Cell Cycle ◽  
Fatty Acids ◽  
T Lymphocytes ◽  
Cell Cycle Progression ◽  
Essential Fatty Acids ◽  
Cycle Progression ◽  
Human T Lymphocytes ◽  
Normal Human ◽  
Definition Of

cAMP inhibits both Ras and Rap1 activation in primary human T lymphocytes, but only Ras inhibition correlates with blockade of cell cycle progression

Blood ◽  
2003 ◽  
Vol 101 (3) ◽  
pp. 998-1006 ◽  
Author(s):  
Thomas Grader-Beck ◽  
Andre A. F. L. van Puijenbroek ◽  
Lee M. Nadler ◽  
Vassiliki A. Boussiotis
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
T Lymphocytes ◽  
T Cell Activation ◽  
Phorbol Ester ◽  
Cell Cycle Progression ◽  
Cell Activation ◽  
Cytokine Production ◽  
Cycle Progression ◽  
Rap1 Activation

Abstract Cyclic adenosine monophosphate (cAMP) is a negative regulator of T-cell activation. However, the effects of cAMP on signaling pathways that regulate cytokine production and cell cycle progression remain unclear. Here, using primary human T lymphocytes in which endogenous cAMP was increased by the use of forskolin and 3-isobutyl-1-methylxanthine (IBMX), we show that increase of cAMP resulted in inhibition of T-cell receptor (TCR)/CD3 plus CD28–mediated T-cell activation and cytokine production and blockade of cell cycle progression at the G1 phase. Increase of cAMP inhibited Ras activation and phosphorylation of mitogen-induced extracellular kinase (MEK) downstream targets extracellular signal–related kinase 1/2 (ERK1/2) and phosphatidylinositol-3-kinase (PI3K) downstream target protein kinase B (PKB; c-Akt). These functional and biochemical events were secondary to the impaired activation of ZAP-70 and phosphorylation of LAT and did not occur when cells were stimulated with phorbol ester, which bypasses the TCR proximal signaling events and activates Ras. Increase of cAMP also inhibited activation of Rap1 mediated by TCR/CD3 plus CD28. Importantly, inhibition of Rap1 activation by cAMP was also observed when cells were stimulated with phorbol ester, although under these conditions Ras was activated and cells progressed into the cell cycle. Thus, TCR plus CD28–mediated activation of ERK1/2 and PKB, cytokine production, and cell cycle progression, all of which are inhibited by cAMP, require activation of Ras but not Rap1. These results indicate that signals that regulate cAMP levels after encounter of T cells by antigen will likely determine the functional fate toward clonal expansion or repression of primary T-cell responses.

4-1BB cross-linking enhances the survival and cell cycle progression of CD4 T lymphocytes

2003 ◽  
Vol 223 (2) ◽  
pp. 143-150 ◽  
Author(s):  
Hyeon-Woo Lee ◽  
Kyung-Ok Nam ◽  
Su K. Seo ◽  
Young H. Kim ◽  
Hyun Kang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Lymphocytes ◽  
Cell Cycle Progression ◽  
Cross Linking ◽  
Cycle Progression

scholarly journals Uncoupling of IL-2 Signaling from Cell Cycle Progression in Naive CD4+ T Cells by Regulatory CD4+CD25+ T Lymphocytes

2004 ◽  
Vol 174 (1) ◽  
pp. 155-163 ◽  
Author(s):  
Christine T. Duthoit ◽  
Divya J. Mekala ◽  
Rajshekkhar S. Alli ◽  
Terrence L. Geiger
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
T Lymphocytes ◽  
Cd4 T Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

2008 ◽  
Vol 89 (4) ◽  
pp. 984-993 ◽  
Author(s):  
Mayra García ◽  
Xiao-Fang Yu ◽  
Diane E. Griffin ◽  
William J. Moss
Keyword(s):  
Cell Cycle ◽  
T Lymphocytes ◽  
Reverse Transcription ◽  
Measles Virus ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Productive Replication

Acute measles virus (MV) infection results in a decrease in plasma human immunodeficiency virus type 1 (HIV-1) RNA levels in co-infected children. An in vitro peripheral blood mononuclear cell (PBMC) culture system was used to assess the mechanisms by which MV blocks HIV-1 replication. MV inhibited proliferation of CD4+ T lymphocytes, the target cell for HIV-1 replication. In the presence of MV, cells did not progress to G1b and S phases, steps critical for the completion of HIV-1 reverse transcription and productive replication. This block in cell-cycle progression was characterized by an increased proportion of CD4+ and HIV-1-infected cells retained in the parental generation in PBMCs co-cultured with MV and HIV-1, and decreased levels of cyclins and RNA synthesis. Early HIV-1 replication was also inhibited in the presence of MV, as measured by reduced expression of a luciferase reporter gene and lower levels of both early (LTR) and late (LTR–gag) DNA intermediates of HIV-1 reverse transcription in the presence of CCR5-tropic HIV-1. The effects of MV on lymphoproliferation and p24 antigen production were reproduced by n-butyrate and hydroxyurea, drugs that block the cell cycle in G1a and G1/S, respectively. It was concluded that MV inhibits HIV-1 productive replication in part by blocking the proliferation of CD4+ T lymphocytes.

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