The role of cbl family of ubiquitin ligases in gastric cancer exosome-induced apoptosis of Jurkat T cells

2009 ◽  
pp. 1-8
Author(s):  
Jing-Lei Qu ◽  
Xiu-Juan Qu ◽  
Ming-Fang Zhao ◽  
Yue-E Teng ◽  
Ye Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Ubiquitin Ligases ◽  
Jurkat T Cells ◽  
Induced Apoptosis

The role of cbl family of ubiquitin ligases in gastric cancer exosome-induced apoptosis of Jurkat T cells

2009 ◽  
Vol 48 (8) ◽  
pp. 1173-1180 ◽  
Author(s):  
Jing-Lei Qu ◽  
Xiu-Juan Qu ◽  
Jing-Lei Qu ◽  
Xiu-Juan Qu ◽  
Ming-Fang Zhao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Ubiquitin Ligases ◽  
Jurkat T Cells ◽  
Induced Apoptosis

Role of MAPK/ERK signaling pathway in gastric cancer exosome-induced apoptosis of Jurkat T cells

2010 ◽  
Vol 18 (19) ◽  
pp. 1969
Author(s):  
Jing-Lei Qu ◽  
Ming-Fang Zhao ◽  
Xiu-Juan Qu ◽  
Ke-Zuo Hou ◽  
You-Hong Jiang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Jurkat T Cells ◽  
Induced Apoptosis

Akt Regulates the Activation-Induced Apoptosis of T Cells Mediated by HIV-1 gp120.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3109-3109
Author(s):  
Appakkudal R. Anand ◽  
Ramesh K. Ganju
Keyword(s):  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Vector Control ◽  
Dominant Negative ◽  
Wild Type ◽  
Jurkat T Cells ◽  
Induced Apoptosis ◽  
Hiv 1

Abstract Multiple mechanisms contribute to the loss of CD4+ T cells in HIV-1 infected individuals. Activation-induced apoptosis of bystander T cells mediated by HIV-1 gp120 is one of the critical mechanisms leading to T cell loss in AIDS. Clinical studies have shown that T cells in the lymph nodes of HIV-1 infected individuals undergo activation-induced apoptosis. In the present study, we used a model where T cells undergo apoptosis after HIV-1 gp120/CD4 cross-linking in conjunction with CD3/T cell antigen receptor activation. We have shown that treatment with HIV-1 gp120 (10 nM) and anti-gp120 MoAb induces approximately 20–25% apoptosis in Jurkat T cells in the presence of immobilized anti-CD3 antibody. However, the molecular mechanism by which HIV-1 gp120 mediates the apoptosis of T cells is still unclear. We have also examined the role of Akt/Protein kinase B in HIV-1 gp120-induced apoptosis. Akt is a cell survival molecule that has been shown to block cell death. We observed a decrease in Akt phosphorylation upon gp120 treatment of Jurkat T cells and peripheral blood mononuclear cells (PBMCs). In contrast, only CD3 stimulation was shown to increase the phosphorylation of Akt. To further confirm the role of Akt in gp120-induced apoptosis, Jurkat T cells were transfected with HA epitope-tagged wild type Akt, dominant-negative Akt that lacks kinase activity, or with a control vector. The transfected cells were treated with gp120 and apoptosis was evaluated by Annexin-PI staining. The T cells expressing wild type Akt showed reduced gp120 apoptosis as compared to the vector control-expressing cells. Conversely, expression of a dominant-negative mutant of Akt accelerated cell death as compared to the vector control. We then further assessed the role of upstream regulators of Akt, such as PI-3 kinase. In this regard, we have shown that inhibition of PI-3 kinase leads to enhanced gp120-induced apoptosis. At present, we are elucidating downstream effectors of the Akt pathway. Taken together, these studies suggest that Akt plays a key role in HIV-1 gp120-induced apoptosis, and that identification of Akt-mediated signaling pathways may provide novel therapeutic targets to combat immune deficiency in AIDS.

scholarly journals The critical role of T cells in glucocorticoid-induced osteoporosis

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Lin Song ◽  
Lijuan Cao ◽  
Rui Liu ◽  
Hui Ma ◽  
Yanan Li ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Steady State ◽  
Side Effects ◽  
Critical Role ◽  
Wild Type ◽  
Receptor Activator ◽  
Steady State Levels ◽  
Induced Apoptosis

AbstractGlucocorticoids (GC) are widely used clinically, despite the presence of significant side effects, including glucocorticoid-induced osteoporosis (GIOP). While GC are believed to act directly on osteoblasts and osteoclasts to promote osteoporosis, the detailed underlying molecular mechanism of GC-induced osteoporosis is still not fully elucidated. Here, we show that lymphocytes play a pivotal role in regulating GC-induced osteoporosis. We show that GIOP could not be induced in SCID mice that lack T cells, but it could be re-established by adoptive transfer of splenic T cells from wild-type mice. As expected, T cells in the periphery are greatly reduced by GC; instead, they accumulate in the bone marrow where they are protected from GC-induced apoptosis. These bone marrow T cells in GC-treated mice express high steady-state levels of NF-κB receptor activator ligand (RANKL), which promotes the formation and maturation of osteoclasts and induces osteoporosis. Taken together, these findings reveal a critical role for T cells in GIOP.

scholarly journals Role for a Glycan Phosphoinositol Anchor in Fcγ Receptor Synergy

1997 ◽  
Vol 139 (5) ◽  
pp. 1209-1217 ◽  
Author(s):  
Jennifer M. Green ◽  
Alan D. Schreiber ◽  
Eric J. Brown
Keyword(s):  
T Cells ◽  
Cell Types ◽  
Polymorphonuclear Neutrophils ◽  
Fcγ Receptor ◽  
Fcγ Receptors ◽  
Jurkat T Cells ◽  
Gpi Anchor ◽  
Transmembrane Anchor ◽  
Activation Motif

While many cell types express receptors for the Fc domain of IgG (FcγR), only primate polymorphonuclear neutrophils (PMN) express an FcγR linked to the membrane via a glycan phosphoinositol (GPI) anchor. Previous studies have demonstrated that this GPI-linked FcγR (FcγRIIIB) cooperates with the transmembrane FcγR (FcγRIIA) to mediate many of the functional effects of immune complex binding. To determine the role of the GPI anchor in Fcγ receptor synergy, we have developed a model system in Jurkat T cells, which lack endogenously expressed Fcγ receptors. Jurkat T cells were stably transfected with cDNA encoding FcγRIIA and/or FcγRIIIB. Cocrosslinking the two receptors produced a synergistic rise in intracytoplasmic calcium ([Ca2+]i) to levels not reached by stimulation of either FcγRIIA or FcγRIIIB alone. Synergy was achieved by prolonged entry of extracellular Ca2+. Cocrosslinking FcγRIIA with CD59 or CD48, two other GPI-linked proteins on Jurkat T cells also led to a synergistic [Ca2+]i rise, as did crosslinking CD59 with FcγRIIA on PMN, suggesting that interactions between the extracellular domains of the two Fcγ receptors are not required for synergy. Replacement of the GPI anchor of FcγRIIIB with a transmembrane anchor abolished synergy. In addition, tyrosine to phenylalanine substitutions in the immunoreceptor tyrosine-based activation motif (ITAM) of the FcγRIIA cytoplasmic tail abolished synergy. While the ITAM of FcγRIIA was required for the increase in [Ca2+]i, tyrosine phosphorylation of crosslinked FcγRIIA was diminished when cocrosslinked with FcγRIIIB. These data demonstrate that FcγRIIA association with GPI-linked proteins facilitates FcγR signal transduction and suggest that this may be a physiologically significant role for the unusual GPI-anchored FcγR of human PMN.

scholarly journals The protective role of miR-223 in sepsis-induced mortality

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Dan Liu ◽  
Zhiding Wang ◽  
Huijuan Wang ◽  
Feifei Ren ◽  
Yanqin Li ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cell Proliferation ◽  
T Cells ◽  
Protective Factor ◽  
Linear Regression Analysis ◽  
Multiple Linear Regression Analysis ◽  
Negative Control ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Jurkat T Cells

Abstract Lymphocyte apoptosis appears to play an important role in immunodysfunction in sepsis. We investigated the role of miR-223 in cell proliferation and apoptosis to identify potential target downstream proteins in sepsis. We recruited 143 patients with sepsis and 44 healthy controls from the Chinese PLA General Hospital. Flow cytometry was used to sort monocytes, lymphocytes, and neutrophils from fresh peripheral blood. A miR-223 mimic and inhibitor were used for transient transfection of Jurkat T cells. Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to assess expression of the miRNAs in cells. Western blot analysis was performed to measure protein expression. We evaluated the cell cycle and apoptosis by using flow cytometry (FCM) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Expression of miR-223 was significantly higher in the survivor group than in the nonsurvivor group. Multiple linear regression analysis revealed that SOFA scores correlated negatively with miR-223 and monocyte counts, with β coefficients (95% CI) of − 0.048 (− 0.077, − 0.019) and − 47.707 (− 83.871, − 11.543), respectively. miR-223 expression also correlated negatively with the percentage of apoptosis in lymphocytes. The rate of apoptosis in the miR-223 mimic group was significantly lower than that of the negative control, with an adverse outcome observed in the miR-223 inhibitor group. We also found that miR-223 enhanced the proliferation of Jurkat T cells and that inhibiting miR-223 had an inhibitory effect on the G1/S transition. We conclude that miR-223 can serve as a protective factor in sepsis by reducing apoptosis and enhancing cell proliferation in lymphocytes by interacting with FOXO1. Potential downstream molecules are HSP60, HSP70, and HTRA.

scholarly journals CD43 cross-linking increases the Fas-induced apoptosis through induction of Fas aggregation in Jurkat T-cells

2006 ◽  
Vol 38 (4) ◽  
pp. 357-363 ◽  
Author(s):  
Hae Jung Kim ◽  
Hyo Jin Park ◽  
Weon Seo Park ◽  
Youngmee Bae
Keyword(s):  
T Cells ◽  
Cross Linking ◽  
Jurkat T Cells ◽  
Induced Apoptosis

scholarly journals Role of plasmacytoid dendritic cells and inducible costimulator‐positive regulatory T cells in the immunosuppression microenvironment of gastric cancer

2014 ◽  
Vol 105 (2) ◽  
pp. 150-158 ◽  
Author(s):  
Xiao‐Mei Huang ◽  
Xiao‐Sun Liu ◽  
Xian‐Ke Lin ◽  
Hang Yu ◽  
Jian‐Yi Sun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Dendritic Cells ◽  
Regulatory T Cells ◽  
Plasmacytoid Dendritic Cells ◽  
Inducible Costimulator

scholarly journals Fas/FasL Pathway Participates in Regulation of Antiviral and Inflammatory Response during Mousepox Infection of Lungs

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Karolina Bień ◽  
Justyna Sokołowska ◽  
Piotr Bąska ◽  
Zuzanna Nowak ◽  
Wanda Stankiewicz ◽  
...  
Keyword(s):  
T Cells ◽  
Inflammatory Response ◽  
Fas Ligand ◽  
Antiviral Response ◽  
Target Cells ◽  
Local Inflammatory Response ◽  
Induced Apoptosis ◽  
Deficient Mice

Fas receptor-Fas ligand (FasL) signalling is involved in apoptosis of immune cells as well as of the virus infected target cells but increasing evidence accumulates on Fas as a mediator of apoptosis-independent processes such as induction of activating and proinflammatory signals. In this study, we examined the role of Fas/FasL pathway in inflammatory and antiviral response in lungs using a mousepox model applied to C57BL6/J, B6. MRL-Faslpr/J, and B6Smn.C3-Faslgld/J mice. Ectromelia virus (ECTV) infection of Fas- and FasL-deficient mice led to increased virus titers in lungs and decreased migration of IFN-γexpressing NK cells, CD4+ T cells, CD8+ T cells, and decreased IL-15 expression. The lungs of ECTV-infected Fas- and FasL-deficient mice showed significant inflammation during later phases of infection accompanied by decreased expression of anti-inflammatory IL-10 and TGF-β1 cytokines and disturbances in CXCL1 and CXCL9 expression. Experiments in vitro demonstrated that ECTV-infected cultures of epithelial cells, but not macrophages, upregulate Fas and FasL and are susceptible to Fas-induced apoptosis. Our study demonstrates that Fas/FasL pathway during ECTV infection of the lungs plays an important role in controlling local inflammatory response and mounting of antiviral response.

scholarly journals Human T-Lymphotropic Virus Type 1 Mitochondrion-Localizing Protein p13II Sensitizes Jurkat T Cells to Ras-Mediated Apoptosis

2005 ◽  
Vol 79 (15) ◽  
pp. 9449-9457 ◽  
Author(s):  
Hajime Hiraragi ◽  
Bindhu Michael ◽  
Amrithraj Nair ◽  
Micol Silic-Benussi ◽  
Vincenzo Ciminale ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Type ◽  
Human Lymphocytes ◽  
Expression Vectors ◽  
Jurkat T Cells ◽  
Reading Frame ◽  
T Lymphotropic Virus ◽  
Adult T Cell Leukemia ◽  
Induced Apoptosis

ABSTRACT Human T-lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia. In addition to typical retroviral structural and enzymatic gene products, HTLV-1 encodes unique regulatory and accessory proteins, including a singly spliced pX open reading frame II (ORF II) product, p13II. We have demonstrated that proviral clones of HTLV-1 which are mutated in pX ORF II fail to obtain typical proviral loads and antibody responses in a rabbit animal model. p13II localizes to mitochondria and reduces cell growth and tumorigenicity in mice, but its function in human lymphocytes remains undetermined. For this study, we analyzed the functional properties of Jurkat T cells expressing p13II, using both transient and stable expression vectors. Our data indicate that p13II-expressing Jurkat T cells are sensitive to caspase-dependent, ceramide- and FasL-induced apoptosis. p13II-expressing Jurkat T cells also exhibited reduced proliferation when cultured at a high density. Furthermore, preincubation of the p13II-expressing cells with a farnesyl transferase inhibitor, which blocks the posttranslational modification of Ras, markedly reduced FasL-induced apoptosis, indicating the participation of the Ras pathway in p13II's influence on lymphocyte survival. Our data are the first to demonstrate that p13II alters Ras-mediated apoptosis in T lymphocytes, and they reveal a potential mechanism by which HTLV-1 alters lymphocyte proliferation.

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