Viewing affirmative mentions of gene expression of Fasl (M. musculus) in T cells

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Mohamood et al. (2007)FasLT-cellMutation of FasL in either compartment interferes with the autoimmune process and prevents onset of diabetes, but FasL expressed in the hematopoietic compartment is the dominant regulator of T-cell homeostasis.
Mohamood et al. (2007)FasLT-cellFurthermore, pathogenesis of diabetes is dependent on normal FasL expression in both compartments, whereas only minimal FasL function is required to maintain T-cell homeostasis.
Nyhus et al. (2001)FasLT cellsThe majority of the data support the theory that FasL expressing tumor cells evade immune surveillance by killing T cells expressing Fas.
Nyhus et al. (2001)FasLT cellsFurther, to determine if the expression of FasL in the environment of the tumor suppresses the humoral antitumor immune response and influences tumor growth, a mouse model lacking T cells was used.
Igney et al. (2003)CD178T cellsMany tumors express the death ligand CD95L (CD178, APO-1L, FasL) and can kill activated T cells in vitro.
Igney et al. (2005)CD95LT cellsTo characterize the effect of CD95L expression of tumor cells on tumor-specific T cells, we established an in vitro system with TCR tg T cells and a model tumor antigen.
Modiano et al. (2004)FasLT cellsWe demonstrate by following the antigen-specific recruitment and subsequent termination of transgenic T cells that activated T cells, including autoreactive cells responsible for CIA, are eliminated within this inflammatory environment through the overexpressed FasL.
Modiano et al. (2004)FasLT cellsThe nature of the inflammatory response, which depends on the Fas ligand being cell bound and not soluble, and the magnitude of FasL expression within the inflammatory milieu are essential for this effect, as arthritogenic inflammation alone resulting from CIA induction is insufficient to ameliorate the disease or eliminate antigen-specific T cells, even upon systemic delivery of soluble FasL.
Wada et al. (2007)FasLT-cellThe growth enhancement of FasL(low) tumors was not observed in T-cell-deficient nude mice, suggesting that FasL expressed in tumors at low levels counteracted against T-cell-dependent antitumor responses.
Tada et al. (2003)FasLT cellsForced expression of FasL in tumors can induce apoptosis of infiltrating Fas-positive T cells; accordingly, tumors can survive in the milieu of systemic immune responses.
Shin et al. (2002)FasLT cellsFas ligand (FasL) expressing cells delete Fas bearing T cells, thereby enabling privileged immune status in the brain.
Hahne et al. (1995)FasLT lymphocytesHere we report that FasL is expressed at similar levels on the surface of activated T lymphocytes from gld and wild-type mice.
Watanabe et al. (1995)FasL mRNAT cellsBy means of in situ hybridization and immunohistochemistry, we identified the cells expressing the FasL mRNA as CD4-CD8- double negative T cells.
Watanabe et al. (1995)FasLT cellsSince FasL is normally expressed in activated mature T cells these results indicate that the double negative T cells accumulating in lpr and gld mice are activated once, and support the notion that the Fas/FasL system is involved in activation-induced suicide of T cells.
Watanabe et al. (1995)FasLT cellsFurthermore, the graft-versus host disease caused by transfer of lpr bone marrow to wild-type mice can be explained by the constitutive expression of the FasL in lpr-derived T cells.
Wasem et al. (2001)FasLT cellsAlthough activation-induced FasL-mediated cytotoxicity in control T cells was sensitive to the immunosuppressant cyclosporin A, we observed that functional FasL expression of GVHD T cells became increasingly cyclosporin A unresponsive.
Nagafuchi et al. (2002)FasLT lymphocytesCONCLUSION: The results suggest that autoreactive B lymphocytes which aberrantly express FasL may kill Fas+ immunoregulatory T lymphocytes.
Tada et al. (2002)FasLT cellPrevious studies however showed that forced expression of FasL in tumors induced neutrophil-mediated inflammatory reactions and accordingly produced T cell independent antitumor effects in the inoculated animals.
Ehl et al. (1996)CD95LCTLTo address the question of whether cytotoxic CD8+ T cells (CTL) activated in vivo are susceptible to cell death mediated by CD95 (Fas/Apo-1) ligand, a recombinant vaccinia virus expressing murine CD95L (vacc CD95L) was constructed, which drives CD95L expression to infected cells.
Tong et al. (2010)FasLT cellsThese results demonstrate that FasL expression on either T cells only or non-T cells only was sufficient for the eventual resolution of airway inflammation, and the prolonged airway inflammation in FasL-deficient Rag(-/-) mice that received Gld T cells was correlated with decreased IFN-gamma production by Gld T cells.
Lowin et al. (1996)FasLT cellsIncubation of MLC-stimulated primary T cells with protein synthesis inhibitors prior to TCR triggering impaired FasL cell surface expression and abolished cytolytic activity, although the cells exhibited an intracellular pool of FasL.
Medana et al. (2001)FasLT cellIn this study, we report that Fas ligand (FasL) expression by neurons is involved in protection against perforin-mediated T cell cytotoxicity.
Toomey et al. (2003)FasLT cellsTumour expression of FasL is thought to disarm responses through the transduction of a death signal in Fas-expressing T cells.
Muruve et al. (1997)FasLT lymphocytesFas ligand (FasL) mediates apoptosis of Fas-bearing cells and is expressed on a limited number of tissues, predominantly activated T lymphocytes.
Bonardelle et al. (2005)FasLT lymphocytesHowever, MRL/lpr autoimmune-prone mice massively overexpress FasL on their T lymphocytes, which render them able to kill Fas+ targets in vitro and in vivo.
Suda et al. (1995)FasLT cellDistribution of FasL mRNA in a panel of cell lines indicated that the FasL expression is rather restricted to the cells of T cell lineage.
Suda et al. (1995)FasLT cellActivation of the splenocytes with the T cell activators such as PMA and ionomycin, Con A, anti-CD3, or even IL-2 alone induced the expression of the FasL.
Müllauer et al. (1998)FasLT-cellIn this study, FasL expression in B- and T-cell non-Hodgkin's lymphomas was investigated by paraffin immunohistochemical analysis.
Reimer et al. (2002)FasLT cellsFasL is predominantly detected in activated T cells and activated natural killer cells, but it is also found on some macrophages/monocytes and on cells of immune privileged tissues [2].
Ryan et al. (2006)FasLT cellIn vitro, T cell activation leads to increased expression of FasL.
Symes et al. (2009)FasLT-cellAs a gene therapy approach to overcome this obstacle, we have created oncoretroviral vectors to overexpress FasL or non-cleavable FasL (ncFasL) on murine T cells of a diverse T-cell receptor repertoire.
Symes et al. (2009)FasLT cellsCo-stimulated T cells expressing FasL, ncFasL and ncFasL/c-FLIP each mediated cytotoxicity in vitro against RM-1 and LNCaP prostate cancer cells.
Pinkoski et al. (2002)FasLT cellHere we used T cell receptor (TCR) transgenic animals to examine the role of inducible expression of nonlymphoid FasL in response to peptide antigen.
Pinkoski et al. (2002)FasLT cellsThese data demonstrate that nonlymphoid FasL is expressed in response to peripheral T cell activation and participates in the regulation of T cells that infiltrate peripheral tissues.
Bossowski et al. (2006)FasLT cellsThe analysis of Fas and FasL expression in thyroid tissues revealed significantly increased percentage of intrathyroidal T cells with CD95+ (p<0.005, p<0.001), CD95L+ (p<0.02, p<0.01) and both CD95/CD95L (ns, p<0.05) expression in comparison to percentages of T cells in patients with HT and NTMG.
Zhang and Xu (2007)FasLT-cellsThere was an apparent decrease in the number of apoptotic Jurkat T-cells after coculture with transfected H22 cells, relative to coculture with FasL-expressing untransfected cells.
Matsuzawa et al. (2002)FasLT cellsTaken together with the fact that DN T cells massively express Fas ligand (FasL), this study implied that FasL overexpressed on DN cells may be involved in the accumulation of DN T cells in LN, LN atrophy and wasting syndrome, and that lprcg Fas, which can bind to Fas ligand but not transduce apoptosis signal into cells, may modulate these pathological conditions by interfering with the binding of FasL to Fas.
Kondo et al. (1997)FasLT cellsThe Fas ligand (FasL) is expressed in activated T cells and induces apoptosis in Fas-bearing cells.
Nagata (1996)FasLT cellsFasL is expressed in activated T cells and natural killer (NK) cells, and works as an effector of these cytotoxic cells to remove the cells infected by virus, or cancer cells.
Zhu et al. (2009)CD95LT cellsRocaglamide sensitizes leukemic T cells to activation-induced cell death by differential regulation of CD95L and c-FLIP expression.
Zhu et al. (2009)CD95LT cellsHere, we show further that Rocaglamide preferentially promotes activation-induced cell death in malignant T cells by differential regulation of c-FLIP and CD95L expression.
Zhu et al. (2009)CD95LT cellsRocaglamide enhances and also prolongs activation-induced JNK activation in malignant T cells leading to downregulation of c-FLIP but upregulation of CD95L expression.
Gregory et al. (2002)FasLT cellsIt has been proposed that the constitutive expression of Fas ligand (FasL) in the eye maintains immune privilege, in part through inducing apoptosis of infiltrating Fas(+) T cells.
Zhang et al. (2005)FasLT lymphocytesCONCLUSION: The expression of FasL is upregulated in colon cancer and the functionally expressed FasL can induce apoptosis of Fas-expressing T lymphocytes.
Bodmer et al. (2002)FasLT-cellsRecently, expression of Fas ligand (FasL) in some non-lymphoid tissue, as in the anterior chamber of the eye, has been hypothesized to play a role in protection of sensitive organs from activated T-cells.
Lamason et al. (2006)FasLT cellsWe therefore considered the possibility that increased estrogen levels during post-pubertal life enhance FasL expression and lead to downstream activation of CD8+ T cells.
Lamason et al. (2006)FasLT cellsWe have shown here that FasL expression on activated CD8+ T cells is influenced by estrogen and have further demonstrated that the culture supernatants from estrogen-activated CD8+ T cells produce growth factors that enhance in vitro immunoglobulin levels.
Lamason et al. (2006)FasLT cellsIt is likely that the transiently elevated levels of estrogen at the time of puberty in males [43,44] may enhance FasL expression on CD8+ T cells.
Wei et al. (2004)FasLT cellsWe previously suggested that CD8(+) T cells promoted resolution of granulomatous experimental autoimmune thyroiditis (G-EAT) at least in part through regulation of Fas ligand (FasL) expression on thyroid epithelial cells.
Wei et al. (2004)FasLT cellsAfter depletion of CD8(+) T cells, G-EAT resolution was delayed, FLIP and FasL were predominantly expressed by inflammatory cells, and few inflammatory cells were apoptotic.
Bobé et al. (1997)FasLT cellsAs a consequence of this defect, activated T cells accumulating in this strain overexpress the FasL and can therefore mediate in vitro Fas-dependent cytotoxicity.
Miyazawa et al. (2002)FasLT cellsIn the clamped kidney, the accumulated intermediate T cells had less cytotoxic activity against tumor cells; however, the expression of the Fas ligand (FasL) increased, indicating a cell-mediated tissue injury via the Fas/FasL system.
Satchell et al. (2004)FasLT cellsBACKGROUND: In the counterattack model of tumorigenesis, it has been proposed that tumours develop resistance to attack from Fas ligand (FasL)-expressing cytotoxic T cells by downregulating Fas (immune escape), while at the same time upregulating FasL expression to induce apoptosis in Fas-expressing T cells (counterattack).
Satchell et al. (2004)FasLT cellsOBJECTIVES: The aim of this study was to examine Fas and FasL expression on tumour cells and infiltrating T cells during the progression of actinic keratoses (AK), the benign precursor lesion, to squamous cell carcinoma (SCC).
Satchell et al. (2004)FasLT cellsRESULTS: FasL-expressing T cells were observed in nine of 19 SCCs, compared with three of 20 AKs (P < 0.05).
Huber et al. (2002)FasLT cellsThis paralleled the expression of very high surface levels of FasL by myocardial gammadelta T cells, as well as their propensity to selectively lyse Th2 virus-specific CD4(+) T cells.
Wagener et al. (2000)FasLT lymphocytesIt is not known whether FasL and TNFalpha, expressed by the recipient's lymphoid or nonlymphoid cells, are essential for the apoptosis of alloreactive T lymphocytes and the induction of allograft acceptance.
Wagener et al. (2000)FasLT cellCONCLUSIONS: These data indicate that: (1) FasL and TNFalpha expression are not obligatory for the induction of long-term allograft acceptance by CTLA4Ig and (2) FasL- and TNFalpha-independent death pathways contribute to alloantigen-driven T cell apoptosis.
Batteux et al. (1999)FasLT lymphocytesIn summary, our results show that FasL expression on thyrocytes may have a curative effect on ongoing EAT by inducing death of pathogenic autoreactive infiltrating T lymphocytes.
Sarcon et al. (2009)CD178T cellsInfused Prf(-/-) LN cells showed less T-cell expansion, normal T-cell activation, and higher proportions of T cells expressing gamma-interferon, tissue necrosis factor-alpha, and Fas ligand CD178, in comparison to infused WT B6 LN cells.
Shioda et al. (2007)Fas-ligandNFATAfter nuclear translocation of NFAT and FKHR, both NFAT and FKHR stimulated expression of Fas-ligand by binding to its promoter region.
Pinkoski et al. (2002)Fas-ligandT cellsThese results define a novel pathway wherein TNFalpha, produced by activated T cells in the intestine, induce Fas-ligand expression in IEC.
Kim et al. (2002)Fas ligandT cellsPrevious reports have demonstrated the ability of antigen-presenting cells (APCs), genetically modified to express Fas ligand (FasL), to inhibit T-cell responses through the induction of apoptosis of antigen-specific T cells.
Mittelstadt and Ashwell (1999)FasLT cellsThus, Egr-2, in addition to Egr-3, regulates FasL expression in activated normal T cells, and Egr-2 is likely to play a direct role in aberrant fasL up-regulation in lpr/lpr and gld/gld CD4(-)CD8(-) T cells.
Georgantas et al. (2000)FasLT cellsWe postulated that coexpression of antigen and FasL within individual antigen-presenting cells would lead to antigen-specific activation of T cells and to their consequent deletion by FasL-mediated AICD.
Kanda et al. (2001)FasLT-cellsVillunger et al. showed that the neoplastic plasma cells express Fas ligand (FasL), which transmits a signal of apoptosis upon ligation to Fas, and suggested that the FasL suppresses the T-cells activated against malignant cells, resulting in escape from tumour immunity.
Sata et al. (2001)FasLT cellIn a rodent model of transplant graft vasculopathy, endothelial overexpression of FasL attenuated T cell and macrophage infiltration at 1 wk posttransplantation.
Tóth et al. (2004)FasLT cellsHere we show that,in the IP-12-7 T cells, RA also induced the expression and DNA binding of nur77, and the cell surface appearance of FasL.
Tóth et al. (2004)FasLT cellsNatural RA also induced the expression of FasL in phytohemagglutinin-activated peripheral murine T cells.
Aung and Graham (2000)FasLT cellsThese data demonstrate that IL-4 increases FasL expression on T cells, resulting in a shift of the mechanism of CTL killing from a dominant perforin-mediated cytolytic pathway to a dominant FasL-mediated cytolytic pathway.
Takeda et al. (1998)FasLT cellsFas ligand (FasL) is highly expressed in testicular tissues and thought to be responsible for protection from allograft rejection by inducing apoptosis of anti-graft activated T cells.
Brunner et al. (1996)FasLT cellSince the immunosuppressive drugs cyclosporin A (CsA) and FK506 block activation-induced apoptosis in T cell hybridomas, we examined whether such compounds affect cell death by interfering with expression of Fas, FasL or both, or whether they block Fas signal transduction.
Brunner et al. (1996)FasLT cellsWe therefore conclude that CsA and FK506 block activation-induced apoptosis in T cell hybridomas predominantly by interfering with activation signals leading to FasL expression and, further, that the regulation of the expression of Fas and FasL on activated T cells is differentially controlled.
Flügel et al. (2000)FasLT-cellHere we report on the neuronal expression of FasL and its potential function in inducing T-cell apoptosis.
Flügel et al. (2000)FasLT cellsThus, FasL expression by neurons in neuroinflammatory diseases may constitute a pivotal mechanism underlying apoptosis of encephalitogenic T cells.
Vacchio and Hodes (2005)FasLT cellExperiments further revealed that expression of FasL by the fetus, but not by the mother, is necessary and sufficient for both components of maternal T cell tolerance to fetal Ags.
Laouar et al. (2000)FasLT cellAbnormalities of the Fas receptor or of FasL expression are associated with excessive T cell proliferation and autoimmunity.
Watanabe et al. (2002)FasLT cellsOral administration of 100 mg of OVA to the mice led to massive cell death of OVA-specific (KJ1-26+)CD4+ T cells by Fas-Fas ligand (FasL)-mediated apoptosis in the liver, which was associated with the emergence of hepatic KJ1-26+CD4+ T cells expressing FasL.
Suarez-Pinzon et al. (1999)FasLT-cellsWe investigated this proposal by examining the expression of FasL and Fas on islet-infiltrating T-cells and beta-cells in relation to beta-cell destruction in a syngeneic islet transplant model in NOD mice.
Suarez-Pinzon et al. (1999)FasLT-cellsTwo-color immunohistochemical assays revealed that FasL was expressed on CD4+ T-cells, CD8+ T-cells, and beta-cells in islet grafts from both diabetic and normoglycemic mice, and the percentage of each type of cell that expressed FasL was greater in islet grafts from normoglycemic compared with diabetic mice.
Suarez-Pinzon et al. (1999)FasLT-cellsThese findings support the concept that cytokine-induced Fas receptor expression on islet beta-cells is a mechanism for their destruction by FasL-expressing CD4+ and CD8+ T-cells and, possibly, by FasL-expressing beta-cells themselves.
Li et al. (2004)FasLT cellsThe results demonstrated that AA T cells abnormally expressed low levels of membrane-bound FasL and contained high levels of intracellular FasL which could be triggered to release by high-dose phytohemagglutinin (PHA) pulse-stimulation.
Li et al. (2004)FasLT lymphocyteThese results indicate that AA T cell is a type of "preactivated" T lymphocyte, characterized by overexpression of FasL, especially intracellular FasL which can be stimulated to release in bioactive exosomes-bound form.
Nguyen and Russell (2001)FasLT cellsSome T cells expressed high levels of FasL yet failed to undergo AICD, while others expressed little FasL and were sensitive.
Szymanska et al. (1999)FasLT cellsGammadelta T cells in both spleen and CNS expressed higher levels of the IL-2rbeta (CD122), as well as Fas and FasL, than alphabeta T cells, suggesting that these cells function as immunoregulatory T cells.
Simpson et al. (1998)Fas-LT cellsThe aims of this study were to determine the relative contribution of perforin and Fas ligand (Fas-L) expression to the cytotoxic action of these T cells and to examine the influence of each pathway in this model of colitis.
Kilinc et al. (2009)FasLT cellsAdoptive transfer of wild-type CD8(+) T cells to FasL-knockout mice restored posttherapy T-suppressor cell elimination from tumors establishing that expression of FasL on CD8(+) T cells was sufficient to promote T-suppressor cell death.
Kilinc et al. (2009)FasLT cellAdoptive transfer of wild-type CD8(+) T cells induced T-suppressor cell death in IFN-gamma-knockout mice confirming that autocrine IFN-gamma was sufficient for CD8(+) T cell FasL expression.
Kim et al. (2005)FasLT cellsOBJECTIVE: In patients with oral squamous cell carcinoma, a high proportion of T cells in the tumor undergo apoptosis, which correlates with Fas ligand (FasL) expression on tumor cells.
Lundy and Boros (2002)FasLT-cellThese results suggest that FasL-expressing, splenic B-1a cells are important mediators of SEA-stimulated CD4(+)-T-cell apoptosis and that maximal FasL expression on B-1a cells is dependent on antigenic stimulation and the presence of IL-4 and IL-10.