Viewing negative mentions of gene expression of Il2 (M. musculus) in T cells

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Rocha et al. (1989)IL2T cellsThe results obtained show that mature T cell growth in vivo is not accompanied by expression of high-affinity interleukin 2 (IL2) receptor in the majority of activated cells, is not abrogated by in vivo administration of anti-IL2 receptor antibodies or enhanced by the in vivo injection of recombinant IL2, and that in vivo growing T cells do not produce detectable amounts of IL2, as evaluated functionally by limiting dilution assays or the presence of IL2 mRNA, detected by Northern blots or in situ hybridization.
Fischbach and Talal (1985)interleukin-2T cellAutoimmune mice bearing the single autosomal recessive gene 1pr are unable to produce the T cell growth factor, interleukin-2 (IL-2).
Kobayashi et al. (1989)IL-2T cellThe antigen-reactive T cell line produces neither IL-2 nor inhibiting factors such as neutralizing factors against preformed IL-2 activity and IL-2 production inhibiting factors, thus the cells are exclusive IL-2 acceptor.
Lopez-Cepero et al. (1988)IL-2T lymphocytesSpleen cell populations enriched for T lymphocytes and depleted of tumor cells by density gradient centrifugation in Ficoll were unable to produce IL-2.
Martins et al. (2008)IL-2T cellsThe conclusion that Blimp-1 represses IL-2 transcription is supported by several observations: (a) Blimp-1–expressing cells do not express IL-2 protein at detectable levels; (b) Blimp-1 mRNA induction correlates with IL-2 mRNA down-regulation; (c) IL-2 protein and steady-state mRNA are elevated in Blimp-1–deficient CD4+ T cells; and (d) endogenous Blimp-1 specifically binds to a regulatory region in the Il2 gene in activated primary CD4+ T cells.
Ishihara et al. (2010)IL-2T cellsBecause the distribution of the Il2 promoter in the liver, where IL-2 is not expressed, was similar to that of the repressed control genes examined in T cells (Figure 4B), the possibility that the Il2 locus was somehow intrinsically different from that of all other loci in its behavior in the SEVENS assay was ruled out.
Alosco et al. (1993)IL-2T cellsIn order to determine whether or not the IL-2 produced by the tumor may be activating tumor cytotoxic effector cells other than B or T cells we have repeated this study using immunodeficient SCID and SCID-beige mice as syngeneic tumor recipients.
O'Neill and Jaworowski (1988)IL-2T cellInternalization of IL-2 by an IL-2-dependent murine T cell lymphoma expressing no detectable cell surface receptors for IL-2.
Melamed and Friedman (1993)IL-2T lymphocytesAt the cellular level, we found that OVA-tolerant T lymphocytes did not produce interleukin-2 (IL-2) nor express IL-2 receptor in response to OVA stimulation in vitro; both observations are indicative of a state of anergy.
Waldmann et al. (1992)IL-2T-cellsIn contrast to resting normal T-cells that do not express high-affinity IL-2 receptors (IL-2R), abnormal T-cells of patients with leukemia-lymphoma, certain autoimmune disorders, and individuals rejecting allografts express this receptor.
Suzuki et al. (1992)IL-2T cellsThese results suggest that the allo-CTL induction in the primary response is IL:-2-dependent and secondary allo-CTL induction is both IL-2 and IL-4-dependent, because unprimed CD4+ T cells produce IL-2, but not IL-4, whereas primed cells produce both IL-2 and IL-4 in response to alloantigens.
Bonneville et al. (1990)IL-2T cellsIn contrast to gamma delta T cells from TLd transgenic mice, gamma delta T cells from TLb transgenic mice did not produce IL-2 and did not proliferate in response to TLb stimulator cells, but they did proliferate in the presence of exogenous IL-2.
Larsson et al. (2000)IL-2T cellsGamma interferon, interleukin-2 (IL-2), RANTES, and the alpha chain of the IL-2 receptor were not expressed at a low dose, whereas a high dose of LPS induced a strong expression of these genes, indicating a dose-dependent activation of T cells.
Suzuki et al. (1986)IL 2T cellsOverall, these results suggest that the SMLR may be a cellular interaction, in which non-T cells stimulate Lyt-1+2- helper T cells to produce IL 3 but not IL 2 or IFN.
Ohta et al. (1987)IL-2T cellThis suggests, taken together with results from previous studies about the cells producing IL-2 and IL-3 by other investigators, that thymosin-alpha 1 exerts its effect at an early stage of T cell differentiation to induce a T cell subpopulation capable of producing IL-3 (but not yet IL-2).
Peppoloni et al. (1987)IL-2T lymphocytesUsing monoclonal antibodies to the IL-2 receptor, we found that Cy-treated T lymphocytes failed to fully express the IL-2 receptor following in vitro stimulation with irradiated tumor cells.
Lieberman and Tsokos (2010)IL-2T cellsT cells were stimulated with the mitogen phytohemagglutinin (PHA) and it was found that they were unable to produce high levels of IL-2; a greater defect was observed in T cells isolated from patients with active disease [6].
Cheever et al. (1984)IL-2T cellsIn contrast to long-term cultured T cells in vivo (which died rapidly in vivo without exogenous IL-2), noncultured donor T cells proliferated in vivo in response to antigen.
Leibson et al. (1981)IL-2-producingT cellThe factor was found in normal Con A Sn that had been depleted of IL-2 by absorption with IL-2-dependent T cells and was absent from Con A-stimulated supernatants of the IL-2-producing T cell hybridoma, FS6-14.13.
Buschman and Skamene (1988)IL-2T cellsThe susceptible animals were found to be T cell-unresponsive since they lacked both proliferative and IL-2 secreting specific T cells.
Lopez-Cepero et al. (1988)IL-2T lymphocytesThis indicates that the failure to detect IL-2 in cells from FLV-infected mice was not due to a dilution of T lymphocytes by tumor cells but was a functional inability to produce IL-2.
Röcken et al. (1991)IL-2T cellsThe factors responsible for the development of CD4+ T cells which produce IL-2 but not IL-4 and cells capable of producing IL-4 but not IL-2 are unknown.
Sileghem et al. (1989)IL 2T cellThe indomethacin-treated co-cultures, which manifest a normal IL 2 production but lack the IL 2 receptors, manifest an impaired DNA synthesis and contain a decreased number of T cell blasts.
Tarleton (1988)IL-2-producingT cellsThese results suggest that the inability of T cells from T. cruzi-infected mice to produce IL-2 in vitro in response to Con A is not due to the lack of IL-2-producing cells, but may be the result of the maturational state of the T cells or to the presence of a suppressor population.
Tanaka et al. (1991)IL-2T cellsFreshly prepared, highly purified T cells from naive mice failed to produce IL-2 in response to soluble anti-CD3 antibody or to Con A and produced only small amounts of IL-2 in response to anti-CD3 coated on the surface of microwells.
Wagner et al. (1988)IL-2T-cellHigh-density (resting) murine Lyt-2+ T cells exposed in vitro to the ligand concanavalin A (Con A), or immobilized F23.1 monoclonal antibody (mAb) recognizing an allotypic determinant on the T-cell receptor (TCR), or high-density (resting) allogeneic B stimulator cells remain IL-2-unresponsive; such cells do not express functional IL-2 receptors unless reconstituted with accessory cells.
Tamura et al. (1990)IL-2T cellThe alloreactive T cell used in the present experiments produced IL-2 in response to soluble anti-CD3 epsilon-chain (anti-CD3) without accessory cell or insoluble antibody carrier.
Steiger et al. (1995)IL-2T cellThese data indicate that 1) IL-2 is not the sole T cell growth factor capable of supporting allograft rejection and 2) expression of IL-4, but not IL-2, during the allograft response does not lead inevitably to tolerance.
Yakova et al. (2005)IL2T cellsMoreover, IL-15 inhibits IL2-mediated activation-induced cell death, and is suspected to both facilitate the persistence of MHC I restricted memory CD8+ T cells involved in the pathogenesis of HAM/TSP, and enhance the survival of self-reactive T cells, leading to the development of autoimmune disease [51].
Ofosu-Appiah et al. (1996)IL-2T cellWhen cultured with either heparan sulfate or Concanavalin A, the T cell clones produced high levels of IL-4 and IL-5 with no detectable IL-2 or IFN-gamma.
Kelley et al. (1986)IL-2T cellsWhile the vast majority of freshly harvested MRL-lpr T cells lack IL-2 receptors (R) as measured by anti-IL-2R monoclonal antibody staining, a large fraction of nonstimulated, cultured (48 hr) MRL-lpr T cells, but not MRL-++ T cells, express IL-2R.
Malek et al. (1984)IL 2T lymphocytesThese experiments demonstrate that IL 2 is the predominant growth factor by which T lymphocytes proliferate, but do not exclude the possibility of an IL 2-independent pathway for growth.
Krämer et al. (1994)IL-2T cellsThus, both in vivo and in vitro, clonal expansion of CD8 T cells can proceed in the absence of IL-2, whereas in peptide-immunized F5 transgenic mice, induction of cytotoxic effector function is IL-2 dependent.
Heeg et al. (1995)IL-2T cellsUpon in vitro restimulation with SEB, CD4+V beta 8+ and CD8+V beta 8+ T cells failed to produce IL-2.
Carlow et al. (2005)IL-2T cellsTo ascertain whether these cytokines were required for P-SelL formation in vivo, TCR transgenic CD8 T cells specific for male Ag (HY) were transferred into male mice under conditions in which either IL-2 and/or IL-15 or IL-12Rp40 were absent.
Furtado et al. (2002)IL-2T cellsWe conclude that T cells with regulatory potential can develop, undergo thymic selection, and migrate to the peripheral lymphoid organs in the absence of IL-2, and do not protect from disease by means of IL-2 secretion.
Cao et al. (1993)IL-2T cellFive of these T cell clones produced both IL-2 and IFN-gamma but not IL-4 after stimulation with either phorbol 12-myristate 13-acetate (PMA) or concanavalin A (Con A).
Colle et al. (1993)IL-2T lymphocytesT lymphocytes from 7-day-infected mice do not proliferate in vitro in response to ConA stimulation, do not produce IL-2 but display high affinity IL-2 receptors on their membrane.
Smith (2004)IL2T cellsHowever, upon subsequent and more extensive testing of IL2 (-/-) mice, it was found that in the absence of IL2, the marked proliferative expansion of LCMV-induced CD8+ T cells was virtually eliminated, the total cytolytic effector capacity was reduced by > 90%, and IFN-?
Smith (2004)IL2T cellsThus, although lymphocyte development during embryogenesis is grossly unperturbed by the absence of IL2, generalized lymphoid hyperplasia ensues after the first several weeks and months of life, and T cells that express activation markers accumulate in the secondary lymphoid tissues.
Röcken et al. (1991)IL-2T cellThe induction of IL-4 and the down-regulation of IL-2 1) were not reproduced with alpha-methyl-mannoside-treated supernatant of Con A-stimulated spleen cells, 2) were not dependent on the presence of large numbers of APC, 3) did not result from differential consumption of lymphokines after restimulation, 4) were not due to a difference in the time course of IL-2 or IL-4 release in either T cell population, and 5) were obtained regardless of the agents used to activate or to restimulate the T cells.
Knoechel et al. (2005)IL-2T cellIn the absence of IL-2, the acute disease is mild because of reduced T cell effector function, but a chronic and progressive disease develops late and is associated with a failure to generate FoxP3(+) regulatory T (T reg) cells in the periphery.
Saron et al. (1991)IL-2T lymphocytesActivated T lymphocytes from mice infected by lymphocytic choriomeningitis virus display high affinity IL-2 receptors but do not proliferate in response to IL-2.
Smith (2004)IL2RsT cellsResting T cells that have not been recently activated via TCR/CD28 do not express detectable high affinity IL2Rs[25].
Hoyle et al. (1998)IL-2T-cellIntracellular cytokine production was assayed by fluorescence-activated cell sorter (FACS), and the expanded T-cell cultures produced IL-2, IFN-gamma, and tumor necrosis factor-alpha (TNF-alpha), but not IL-4.
Clements et al. (1993)IL-2T cellsThis subset of T cells does not proliferate or produce IL-2 in response to mitogenic signals or TCR-CD3 ligation.
Seder et al. (1991)IL2T cellsT cells from primed donors showed a striking inhibition in the frequency of IL4-producing cells in response to anti-CD3 when IL2 was not present.
Alcina and Fresno (1985)interleukin 2T cellMoreover, they were unable to produce detectable amounts of the growth factor required for T cell proliferation, interleukin 2.
Ragin et al. (2005)IL-2T cellsg/ml SEB concentration (Fig. 2bi), ITK null T cells made very little IL-2, and the small amount of IL-2 that was made was only at the highest concentration of SEB tested (5 ?
Kirkman et al. (1985)IL-2T cellsAs the IL-2 receptor is not present on resting T cells, it offers an attractive target for potentially specific immunosuppressive therapy.
McDevitt (2003)IL-2T cellsThus, GAD65 specific TCR transgenic T cells (1) must express a second a chain to survive negative selection, (2) produce IL-2 and IFN-gamma, and (3) have a mildly protective effect on transfer of diabetes with diabetogenic spleen cells.
Kobayashi et al. (2001)IL-2T cellsType 1 cytokines (IFN-gamma and IL-2), however, were not produced by these T cells after the same stimulation.
Li et al. (1998)IL-2T cellHence, a T cell dependent allograft rejection enabled by rapamycin-sensitive signals or signals mediated by binding of the gamma c chain occurs in the absence of both IL-2 and IL-4.
Takenaka et al. (2001)IL-2T cellsDonor-derived CD4+ T cells failed to proliferate in response to host alloantigens, and both donor- and host-derived T cells were unable to produce IL-2 in response to concanavalin A stimulation, suggesting that SEB treatment induced a general immunosuppressive state.
Heinzel et al. (1993)IL-2T cellOther cytokines or activation pathways that are either IL-2-independent or synergistic with low levels of IL-2 may account for the appearance of curative T cell responses during treatment with anti-IL-2 antibodies.
Seixas et al. (2002)IL-2T cellThe large gammadelta T cell expansion normally observed in infected B cell-deficient mice did not take place in the absence of IL-2, and double-knockout mice lacking both B cells and functional IL-2 were highly susceptible to lethal infection with P. c. chabaudi.
Ragin et al. (2005)IL-2T cellThe data suggest that the inability of T cell lacking ITK to produce IL-2 cannot be overcome by SAG stimulation, and that perturbing T cell activation pathways leading to IL-2 production does not necessarily lead to improved responses to SEB toxicity.
Guerne et al. (1983)IL 2T cellIPA and MAF were not produced with the same kinetics and in the same T cell concentration conditions as IL 2 and TRF.
McKay et al. (1999)IL-2T cellsWe employed a TCR transgenic mouse, bearing the 2C TCR, providing adequate numbers of homogenous peripheral T cells to study biochemical aspects of T cell unresponsiveness in vivo. 2C mice exposed to semiallogeneic lymphocytes (H-2b x H-2d) experienced prolonged H-2d cardiac allograft survival, and cells from these mice did not proliferate or make IL-2 in response to alloantigen (H-2d).
Moriyama et al. (1995)IL-2T cellsThe asialoGM1+CD4+ T cells produced IL-2 and IFN-gamma in primary culture without stimulant but did not proliferate.
Bradley et al. (1991)IL-2T cellsWhen restimulated with specific antigen in vitro, CD4+ T cells from mice primed 5 to 7 days previously by subcutaneous administration of keyhole limpet hemocyanin (KLH) in adjuvant, produced high levels of interleukin 2 (IL-2), IL-4, and IL-3, and little or no interferon gamma (IFN-gamma) or IL-5.
Brimnes et al. (2003)IL-2T cellsIn the absence of influenza, these OVA-specific T cells produced little IL-2, IL-4, IL-10, and IFN-gamma, but with infection, both CD4+ and CD8+ T cells made high levels of IL-2 and IFN-gamma.
Perrin et al. (2000)IL-2T cellsSplenic T cells from mice with EAM produced TNF-alpha and IL-6 but no IL-2.
Perrin et al. (2000)IL-2T cellsConversely, EAE-derived splenic T cells produced TNF-alpha and IL-2 but no IL-6.
Kobie et al. (2006)IL-2T cellCD73 (5'-ectonucleotidase) is expressed by two distinct mouse CD4 T cell populations: CD25+ (FoxP3+) T regulatory (Treg) cells that suppress T cell proliferation but do not secrete IL-2, and CD25- uncommitted primed precursor Th (Thpp) cells that secrete IL-2 but do not suppress in standard Treg suppressor assays.
Carrier et al. (2007)IL-2T cellsTo address this issue, we generated a TGF-beta1-transgenic (Tg) mouse in which TGF-beta is linked to the IL-2 promoter and T cells transiently overexpress TGF-beta upon TCR stimulation but produce little or no IL-2, IL-4, IL-10, IL-13, or IFN-gamma.
Parenteau et al. (1992)IL-2T cellsHigh-affinity IL-2 receptors are expressed by T cells activated in response to foreign histocompatibility antigens but not by normal resting T cells.
Bendle et al. (2007)IL-2T cellsWhile non-tolerant control T cells of Agneg mice secreted IL-2 upon peptide stimulation, no IL-2 was detectable when the T cells of Agpos mice were stimulated (Figure 2B).
Hattori et al. (2006)IL-2T cellsSera from TG nude mice with keratitis reacted with alpha-internexin on Western blot analysis, and the T cells of these mice on stimulation with alpha-internexin exhibited proliferation responses and produced IL-2, IFN-gamma, and TNF-alpha, but not IL-4 or IL-5.
Xu et al. (1997)IL-2T cellA long-term uveitogenic T cell line, initially derived in the presence of IL-12, produced IFN-gamma and IL-2, but not IL-4, and was CD4+ (Th1-like).
Quill et al. (1994)IL-2T cellThese data indicate that T cell clonal anergy results in profound inhibition of proliferative responses, since the autocrine growth factor, IL-2, is not produced, and the APC-derived cytokine, IL-12, is not an effective stimulus for anergic T cell proliferation.
Rosendahl et al. (1996)IL-2T cellsT cells responded well to 3 daily injections of C215Fab-SEA and then gradually entered a hyporesponsive state, characterized by a reduced ability to produce IL-2, TNF-alpha and IFN-gamma and failure to mediate cytotoxicity in vitro.
Hattori et al. (1998)IL-2T cellThe BALB/c splenic H32+ CD4+ T cell subset produced few cytokines except IL-2, thus corresponding to naive ThP-type cells.
Kubota et al. (1994)IL-2T cellsThese results indicate that the massively accumulating lymphocytes of MRL/l mice have a property characteristic of activated T cells, although they express little surface CD4 or CD8 and do not produce IL-2.
Frosch et al. (1996)IL-2T cellsWhen BI/O4.1 T cells were used as APC, KIII5 cells produced IL-2, but did not proliferate.
Croitoru et al. (1994)IL-2T cellsWe conclude that the lack of CD5 defines a unique subset of intraepithelial T cells expressing either TCR gamma delta or alpha beta that include potentially autoreactive cells that remain anergic in the absence of IL-2.
Quanquin et al. (1999)interleukin 2T cellsThis population of T cells also produces both IFN-gamma and interleukin 2 (IL-2) but not IL-4 or IL-5 when incubated with spleen cells stimulated with TolT antigen, indicating that they are of the T-helper 1 type.
Graham et al. (2006)IL-2T cellsIn contrast to SLAM-/- and SAP-/- mice, T cells from Ly9-/- mice proliferate poorly and produce little IL-2 after suboptimal stimulation with anti-CD3 in vitro.
Takeuchi et al. (1998)IL-2T cellsP518-529-specific T cells produced IL-2 and IFN-gamma, but not IL-4 or IL-10, whereas P1182-1194-specific T cells produced IL-4 and IL-10, but not IL-2 or IFN-gamma Adoptive transfer of these peptide-specific T cells into naive BALB/c nude mice resulted in development of uveoretinitis only in the P518-529 case.
Kashiwada et al. (2006)IL-2T cellsHowever, these T cells did not proliferate or produce IL-2 after stimulation.
Gysemans et al. (2000)IL-2T-cellT-cell cytokines (IL-2, IL-4, IL-10, and gamma-interferon) were absent in all mice until 48 h after transplantation.
Min et al. (2001)IL-2T cellsIn prior studies, we found that exposure of newborn mice to Ig-PLP1, a chimera expressing the encephalitogenic proteolipid protein (PLP) sequence 139-151, induced deviated Th2 lymph node cells producing IL-4 instead of IL-2 and anergic splenic T cells that failed to proliferate or produce IFN-gamma yet secreted significant amounts of IL-2.
Tsang et al. (2006)IL-2T cellThe CD4(+)CD25(+) T cell lines were anergic after TCR stimulation and produced little cytokine such as IL-2 and IFN-gamma.
Jump and Levine (2002)IL-2T cellsUpon stimulation, only CD45RB(low)CD4(+) PP T cells produce IL-10, whereas secretion of IL-2, IL-4, and IFN-gamma was not detected.
Naiki et al. (1992)IL-2T cellAll of the autoreactive cloned T cell lines produce significant IL-4 but no detectable IL-2 or IFN-gamma.
Mayack and Berg (2006)IL-2T cellsSpecifically, activated Jak3(-/-) CD4(+) T cells produce IL-10, TGF-beta, and IFN-gamma, but not IL-2 or IL-4, and are unable to proliferate in vitro.
Wood et al. (1990)IL-2T-cellConcanavalin A (Con A)-induced supernatant (SN) from the T-cell clone D10.G4, which contains high concentrations of interleukin-3 (IL-3), IL-4 and IL-5, but lacks IL-1, IL-2 and interferon (IFN), markedly increased the proportion of CD4+CD8- cells, and decreased the proportion of CD4+CD8+ cells.