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

Full-text article links are indicated by after the article reference.

Document Target Regulator Anatomy Sentence
Green and Flavell (2000)TNFalphaT cellsFurther, we have described an interval between 21 and 25 days following initiation of TNFalpha expression where the fate of islet-reactive T cells is decided.
Li et al. (2006)TNFalphaT cellsThese studies demonstrate that the production of TNFalpha in activated B cells is regulated differently than in activated T cells, and these differences may allow for the selective inhibition of TNFalpha in various autoimmune diseases depending on the mechanism of action of the selected anti-TNFalpha therapy.
Brown et al. (2004)tumor necrosis factor-alphaT cellsThe pathogenesis of acute graft-versus-host disease (aGVHD) includes tumor necrosis factor-alpha (TNFalpha) expression by macrophages and T cells.
Tsytsykova and Goldfeld (2000)TNF-alphaT cellsThese results demonstrate that NFATp is an essential activator of immediate early TNF-alpha gene expression in T cells and they present in vivo evidence of the inducer- and cell type-specific regulation of TNF-alpha gene expression.
Nansen et al. (1997)TNF-alphaT cellHyperproduction of TNF-alpha was temporally correlated with virus-induced production of interferon-gamma (IFN-gamma); only marginally increased IFN-gamma and TNF-alpha production was observed in LCMV-infected, T cell-deficient mice and in mice infected with vesicular stomatitis virus, a virus that induces much less T cell activation than does LCMV.
Held et al. (1990)tumor necrosis factor alphaT cellsA considerable portion of cells expressing tumor necrosis factor alpha appear to be CD4+ T cells.
Ewing et al. (2007)tumor necrosis factor alphaT-cellDonor CD4+ T-cell production of tumor necrosis factor alpha significantly contributes to the early proinflammatory events of graft-versus-host disease.
Ewing et al. (2007)TNFalphaT cellsWe investigated to what extent donor T cells contribute to TNFalpha production.
Ewing et al. (2007)TNFalphaT cellsRESULTS: Analysis of serum TNFalpha kinetics in recipients of allogeneic B6 wild-type BM and wild-type T cells revealed that TNFalpha levels peaked around day 7 after allo-BMT, whereas TNFalpha was undetectable in syngeneic controls.
Ewing et al. (2007)TNFalphaT cellsFurther exploration showed that specifically donor CD4(+) but not CD8(+) T cells were the primary donor cell source of TNFalpha at this early time point; numbers of TNFalpha expressing splenic CD4(+) T cells were higher than CD8(+) T cells 7 days after allo-BMT, and maximal serum TNFalpha levels were detected following allo-BMT with only CD4(+) T cells compared to levels found in allogeneic recipients of only wild-type CD8(+) or to only CD4(+) TNFalpha(-/-) T cells.
Ewing et al. (2007)TNFalphaT cellsCONCLUSION: Our data demonstrate that in addition to residual host cells donor CD4(+) T cells significantly contribute to the proinflammatory cytokine milieu engendered early after allo-BMT through the production of TNFalpha.
Phares et al. (2007)TNF-alphaT cellsMoreover, the induction of TNF-alpha expression in CNS tissues by RV infection has no impact on BBB integrity in the absence of T cells.
Iversen et al. (2002)TNF-alphaT cellsIn these mice, TNF-alpha/Fas expression was increased in bone marrow natural killer (NK) and T cells, and these lymphocytes showed increased cytolytic activity in vitro against progenitor cells.
Tran et al. (2005)TNFalphaT cellsT cells also interact with monocytes and macrophages and cytokine-activated T cells may be, especially, suited to trigger production of the important cytokine TNFalpha by synovial macrophages.
Zou et al. (2002)TNFalphaT cellsWhile infliximab induced a downregulation of the production of the T-helper 1-cytokines IFNgamma and TNFalpha, etanercept treatment triggered rather an upregulation of these cytokines secreted by T cells after in vitro stimulation.
Dahlén et al. (1998)TNF-alphaT cellsHowever, on immunohistochemical analysis of TNF-alpha expression in islets, we are able to show that the staining pattern of TNF-alpha resembles that of dendritic cells (DC) and macrophages (Mphi) rather than T cells and that TNF-alpha is expressed in islets at the very early stages of insulitis when no T cells are detected.
Minematsu et al. (2007)TNF-alphaNFATConsequently, we examined the role of nuclear factor of activated T cells (NFAT) in TNF-alpha production.
Sawyer et al. (2000)TNF-alphaT cellThe 12j cell line, contrasted with other macrophage hybrids that do not respond to Be-stimulation, may provide a useful tool to evaluate the mechanisms by which Be stimulates macrophage cytokine production, and by which T cell derived IFN-gamma amplifies TNF-alpha production in granulomatous diseases.
Ito et al. (2002)TNF-alphaT cellEstrogen inhibits systemic T cell expression of TNF-alpha and recruitment of TNF-alpha(+) T cells and macrophages into the CNS of mice developing experimental encephalomyelitis.
Ito et al. (2002)TNF-alphaT cellsE2 treatment also had profound inhibitory effects on expression of TNF-alpha by splenic CD4(+) T cells, including those responsive to MOG 35-55 peptide.
Imose et al. (2004)TNF-alphaT lymphocytesThese findings were supported by the results in which leflunomide administration decreased the number of T lymphocytes infiltrating the liver as well as inhibiting their production of TNF-alpha.
Cenci et al. (2000)TNF-alphaT-cellEstrogen deficiency induces bone loss by enhancing T-cell production of TNF-alpha.
Cenci et al. (2000)TNF-alphaT cellsThese findings demonstrate that the ability of estrogen to target T cells, suppressing their production of TNF-alpha, is a key mechanism by which estrogen prevents osteoclastic bone resorption and bone loss.
Zhang et al. (2006)TNFalphaT lymphocyteThe T lymphocyte transformation capacity was tested by MTT assay, the TNFalpha and IL-2 production were measured by LDH kits.
Zhang et al. (2006)TNFalphaT lymphocyteNobiletin could stimulate T lymphocyte transformation and the production of TNFalpha and IL-2.
Lau et al. (2009)TNFalphaT cellMETHODS: Using a murine model of KD, we established and validated several in vitro techniques to reflect 3 key steps involved in disease pathogenesis, as follows: thymidine incorporation to evaluate T cell activation, enzyme-linked immunosorbent assay to measure tumor necrosis factor alpha (TNFalpha) production, and real-time polymerase chain reaction to examine TNFalpha-mediated expression of matrix metalloproteinase 9 (MMP-9).
Grewal et al. (1996)TNF alphaT cellsLocal expression of transgene encoded TNF alpha in islets prevents autoimmune diabetes in nonobese diabetic (NOD) mice by preventing the development of auto-reactive islet-specific T cells.
Grewal et al. (1996)TNF alphaT cellsThese data establish a mechanism of TNF alpha action and provide evidence that local expression of TNF alpha protects NOD mice from autoimmune diabetes by preventing the development of autoreactive islet-specific T cells.
Holzheimer et al. (2002)TNFalphaT cellThe results showed that seven days after sham or thermal injury both T cell IL-2 and adherent cell TNFalpha production were altered by time of injury or time of cell harvest.
Lider et al. (1995)tumor necrosis factor alphaT-cellThis inhibition of T-cell mediated inflammation in vivo was associated with an inhibitory effect of the disaccharide on the production of biologically active tumor necrosis factor alpha (TNF-alpha) by activated T cells in vitro; the trisulfated disaccharide did not affect T-cell viability or responsiveness generally.
Brehm et al. (2007)TNF-alphaT cellsRapid quantification of naive alloreactive T cells by TNF-alpha production and correlation with allograft rejection in mice.
Brehm et al. (2007)TNF-alphaT cellsNaive alloreactive T cells were identified by the production of TNF-alpha after a 5-hour in vitro stimulation with alloantigen and were distinguished from effector/memory alloreactive T cells by the inability to produce IFN-gamma.
Brehm et al. (2007)TNF-alphaT cellsWe conclude that rapid production of TNF-alpha can be used to quantify naive alloreactive T cells, that it is abrogated after the induction of tolerance, and that it is a potential tool to predict allograft rejection.
Dohi et al. (1993)TNF alphaT cellsAn immunoprecipitation study revealed that these T cells expressed TNF alpha molecules of 26 kDa, but not of 17 kDa, suggesting that tumour cell lysis was caused by membrane-integrated integrated TNF alpha molecules.
Suzuki et al. (2010)TNFT-cell(CCL4), platelet-derived growth factor (PDGF-bb), regulated upon activation, normal T-cell expressed and secreted (RANTES, CCL5), tumor necrosis factor (TNF)-a, and vascular endothelial growth factor (VEGF).
Young et al. (2010)TNFT cellsIn this regard, we saw a significant increase in CD4+ T cells producing TNF-?
Isoda et al. (2010)TNFT cellsMoreover, IL-1Ra(-/-) T cells produced much higher levels of tumor necrosis factor (TNF)-alpha in culture supernatants after anti-CD3 antibody stimulation compared to wild-type mice (P<0.001).
Barin et al. (2010)TNFT cellsWe observed multiple apoptotic defects in caspase activity, and the expression of TNF superfamily members on CD4(+) T cells.
Ascon et al. (2009)TNF-alphaT cellThere was a significant upregulation of IL-1beta, IL-6, TNF-alpha, IFN-gamma, MIP-2, and RANTES expression, measured by real-time PCR, 6 weeks after unilateral renal ischemia, further indicating T cell activation.
de Alencar et al. (2009)tumor necrosis factorT cellsIn spite of a normal numeric expansion, specific CD8(+) T cells presented several functional defects detected in vivo (cytotoxicity) and in vitro (simultaneous expression of CD107a/IFN-gamma or IFN-gamma/tumor necrosis factor alpha) paralleled by a decreased expression of CD44 and KLRG-1.
Ramana et al. (2009)TNF-alphaT cellsWe have used a mouse model to specifically investigate the role of antiviral CD8(+) T cells in this injury, and have found that the critical effector molecule is TNF-alpha expressed by the T cells upon antigen recognition.
Magalhaes et al. (2008)tumor necrosis factorT-cellsDetection of intracellular cytokine production (interleukin-2, interferon-gamma, and tumor necrosis factor-alpha) upon phorbol 12-myristate 13-acetate-ionomycin stimulation in CD8alphaalpha+ and CD8alphabeta+ T-cells revealed that CD8alphaalpha+ T-cells show a unique cytokine production pattern (tumor necrosis factor-alpha and interferon-gamma production) as compared with CD8alphabeta+ T-cells.
Jiang et al. (2008)tumor necrosis factorT cellsThis may due to the induction of a Th2-bised immune response specified with decreased expression of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma but increased expression of IL-10 and IL-4 in serum and heart tissue, more IL-4 but less IFN-gamma secreting splenic CD4+ T cells, an immunoglobulin G1 isotype switch, increased expression of GATA-3 and low proliferation of CD8+ T cells, without significant change of virus titer in heart tissue.
Blossom et al. (2008)TNF-alphaT cellsThe immunoregulatory effects of TCE involved a redox-associated promotion of T cell differentiation in the thymus that preceded the production of proinflammatory cytokines, IL-2, TNF-alpha, and IFN-gamma by mature CD4+ T cells.
Banerjee et al. (2008)tumor necrosis factorT cellInduction of messenger ribonucleic acid for the chemokines, macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta and regulated upon activation, normal T cell expressed and secreted indicated a strong bias of PIL for type 1 polarization that was supported by the intracellular expression and release of tumor necrosis factor (TNF)-alpha and IL-12.
Denton et al. (2007)TNF-alphaT cellsWhile IL-12 appeared to have no notable effect on either virus growth or on CD8+ T cell response profiles, the absence of IL-18 was associated with delayed virus clearance from the lung and, despite normal numbers, a significantly reduced production of IFN-gamma, TNF-alpha, and IL-2 by epitope-specific CD8+ T cells.
Teng et al. (2007)tumor necrosis factorT cellsThis therapy comprised an agonistic mAb reactive with tumor necrosis factor-related apoptosis-inducing ligand receptor (DR5), expressed by tumor cells, an agonistic anti-CD40 mAb to mature dendritic cells, and an agonistic anti-4-1BB mAb to costimulate CD8(+) T cells.
Coler et al. (2007)tumor necrosis factorT cellsAnalysis of the cellular immune responses of immunized, uninfected mice demonstrated that the vaccine induced a significant increase in CD4(+) T cells producing gamma interferon, interleukin 2, and tumor necrosis factor cytokines, indicating a Th1-type immune response.
Lin et al. (2007)tumor necrosis factorT-cellAAV2/8 produced a vibrant CD8(+) T-cell effector response characterized by coexpression of gamma interferon and tumor necrosis factor alpha as well as in vivo cytolytic activity.
Ismail et al. (2007)tumor necrosis factorT cellsInfection with gram-negative monocytotropic Ehrlichia strains results in a fatal toxic shock-like syndrome characterized by a decreased number of Ehrlichia-specific CD4(+) Th1 cells, the expansion of tumor necrosis factor alpha (TNF-alpha)-producing CD8(+) T cells, and the systemic overproduction of interleukin-10 (IL-10) and TNF-alpha.
West et al. (2006)TNF-alphaT cellsAllospecific CD8+ IFN-gamma+ T cells were detected in airway allografts, with significant coexpression of TNF-alpha and granzyme B.
Zhang et al. (2006)TNFT cellsActivated STAT5a/b-/- T cells showed increased expression of proapoptotic (caspases, DNA repair genes, TNF/TNFR-associated factor family genes) and decreased antiapoptotic mRNAs in microarrays, while Western blots confirmed reduced antiapoptotic Bcl-2 and elevated proapoptotic Bax protein expression.
Sjöö et al. (2006)tumor necrosis factorT cellsTreatment with treosulfan induced only interleukin-2 production in spleen cells for a short time and had no significant effect on synthesis of tumor necrosis factor-alpha and/or interferon-gamma as compared with that observed in splenic T cells isolated from mice treated with either busulfan or cyclophosphamide.
Kanai et al. (2006)tumor necrosis factorT cellRESULTS: Mice reconstituted with CD4CD45RB but not CD4CD25 T cells developed a wasting disease, with severe infiltrates of B cell aggregates as well as T cells, macrophages, and dendritic cells into the colon and elevated levels of interferon-gamma, tumor necrosis factor-alpha, interleukin (IL)-4, IL-5, and IL-10, by 7 weeks after T cell transfer.
Vogler et al. (2006)tumor necrosis factorT-cellThe T-cell proliferative response to the specific antigen was increased in UCP2-deficient mice compared with littermate controls, and CD4 cells of UCP2 knockout mice produced significantly higher levels of pro-inflammatory cytokines, eg, tumor necrosis factor-alpha and interleukin-2, resulting from a Th1 response.
Taraban et al. (2006)TNFT cellIn this study, we investigate the role of CD70, a member of the TNF superfamily that is expressed on activated DC, in CD4+ Th-dependent and -independent CD8+ T cell responses.
Fonseca et al. (2006)tumor necrosis factorT cellsIL-12 co-administration with pCI/Sm14 induced a significant production of nitric oxide in splenocyte culture supernatants and also lymphocyte suppression, with reduced percentage of T cells producing IFN-gamma and tumor necrosis factor-alpha.
Wang and Murphy (2006)TNF-alphaT-cellsT cells recovered from recipients of CCR5 KO cells produced more IFN-gamma and TNF-alpha and proliferated to a T-cell at a significantly higher level than T cells from recipients of WT cells, indicating that CCR5 plays a role in downregualting donor alloreative CD8(+) T-cells expansion.
Rey-Ladino et al. (2005)tumor necrosis factorT cellsDC exposed to live EBs acquired a mature DC morphology; expressed high levels of major histocompatibility complex (MHC) class II, CD80, CD86, CD40, and ICAM-1; produced elevated amounts of interleukin-12 and tumor necrosis factor alpha; and were efficiently recognized by Chlamydia-specific CD4+ T cells.
Woods et al. (2005)tumor necrosis factorT cellRESULTS: Intranasal delivery of pG-IL-10 significantly delayed arthritis onset and reduced disease severity in the prophylactic group and early therapy group, reduced cellular infiltration and bone loss in the early therapy group, and reduced T cell proliferation in response to collagen on days 31 and 65 in these two groups, with a significant reduction in tumor necrosis factor alpha production on day 65.
Rossi-George et al. (2005)tumor necrosis factorT-lymphocytesStaphylococcal enterotoxin A (SEA) is a microbial superantigen that activates T-lymphocytes and induces production of various cytokines, including tumor necrosis factor-alpha (TNFalpha).
Boyman et al. (2004)tumor necrosis factorT cellsOur observations highlight the importance of resident T cells in the context of lesional tumor necrosis factor-alpha production during development of a psoriatic lesion.
Welniak et al. (2004)TNF-alphaT-cellT cells recovered from recipients of CCR5 KO cells produced more IFN-gamma and TNF-alpha and proliferated to a T-cell mitogen at a significantly greater level then T cells from recipients of WT cells, indicating that CCR5 plays a role in downregulating donor alloreactive CD8+ T-cell expansion.
Liu et al. (2004)tumor necrosis factorT cellsThe systemic production of tumor necrosis factor alpha, interferon gamma, and interleukin-6 was attenuated in mice either by a cell-permeant cyclized form of SN50 peptide or by a transgene whose product suppresses the nuclear import of transcription factor nuclear factor kappa B in T cells.
Friedman et al. (2004)tumor necrosis factorT cellsThe progeny of old T cells reisolated after transplantation expressed type 1 cytokines (interferon-gamma and tumor necrosis factor-alpha) at a lower frequency than young cells and had decreased cytolytic function against H-2(k)-bearing target cells.
Akabane et al. (2004)tumor necrosis factorT cellMoreover, TAS-3-124 inhibited the production of proinflammatory cytokines including interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-6 but not T cell derived cytokines in mice.
Curry et al. (2004)tumor necrosis factorT-cellBACKGROUND: CD134 (OX40) is a member of the tumor necrosis factor receptor superfamily that is expressed as a late event in T-cell activation and contributes to the generation of immunologic memory.
Kovacs et al. (2004)tumor necrosis factorT-cellTopics were (1) T-cell activation after chronic ethanol ingestion in mice, (2) effect of ethanol consumption on the severity of acute viral-mediated pancreatitis, (3) ethanol and alveolar macrophage dysfunction, (4) impaired intestinal immunity and barrier function: a cause for enhanced bacterial translocation in alcohol intoxication and burn injury, (5) immune consequences of the combined insult of acute ethanol exposure and burn injury, (6) consequences of alcohol-induced dysregulation of immediate hemodynamic and inflammatory responses to trauma/hemorrhage, (7) regulation of tumor necrosis factor-alpha production by Kupffer cells after chronic exposure to ethanol, (8) acute exposure to ethanol and suppression of cytokine responses induced through Toll-like receptors, and (9) inhibition of antigen-presenting cell functions by alcohol: implications for hepatitis C virus infection.
Kristensen et al. (2004)TNF-alphaT cellsOverall, virus-specific CD8(+) T cells produce a similar range of cytokines (IFN-gamma, TNF-alpha, IL-2, GM-CSF, RANTES, MIP-1alpha and MIP-1beta) as CD4(+) T cells, but the relative distribution of cytokine-producing subsets is different.
Makobongo et al. (2003)tumor necrosis factorT cellWe generated CD4(+) T cell lines to fractions of native antigens from the blood stages of the rodent parasite, Plasmodium yoelii, and identified fraction-specific T cells that had a Th1 phenotype (producing IL-2, IFN-gamma, and tumor necrosis factor-alpha, but not IL-4, after antigenic stimulation).
Ajuebor et al. (2003)TNF-alphaT cellsCon A-induced hepatitis is a liver-specific inflammation mediated by activated T cells and is driven by an up-regulation of the hepatic expression of TNF-alpha, IFN-gamma, and IL-4.
Musgrave et al. (2003)TNFT cellsAnti-CD2 mAb did not affect expression of Fas ligand and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) by anti-CD3-activated T cells.
Ilangumaran et al. (2003)TNF-alphaT cellsIL-15 strongly induces TNF-alpha production in SOCS1-deficient CD8+ T cells, indicating that SOCS1 is also a critical regulator of CD8+ T cell activation by IL-15.
Weir et al. (2003)tumor necrosis factor-alphaT cellsAntigen-specific T cells from IL-5(-/-) mice produced IFN-gamma and tumor necrosis factor-alpha, but no IL-4 or IL-10, indicating that a predominant T(h)1 environment was induced following immunization.
Ye et al. (2002)tumor necrosis factorT cellsLIGHT (TNFSF14), a tumor necrosis factor superfamily member expressed by activated T cells, binds to herpes virus entry mediator (HVEM) which is constitutively expressed by T cells and costimulates T cell activation in a CD28-independent manner.
Trama et al. (2002)TNF-alphaT cellsExpression of the TNF-alpha gene, a putative NFAT5 target, was not altered in transgenic T cells.
Song et al. (2002)tumor necrosis factorT cellIn those studies, we demonstrated that the increased CD57(+) T cell population rapidly produces interferon-gamma (IFN-gamma) and tumor necrosis factor alpha, independent of a second signal requirement, consistent with an increased effector T cell population.
Kiani et al. (2001)tumor necrosis factorT cellsTranscription factors of the nuclear factor of activated T cells (NFAT) family are thought to regulate the expression of a variety of inducible genes such as interleukin-2 (IL-2), IL-4, and tumor necrosis factor-alpha.
Tanaka and Noda (2001)TNF-alphaT cellsIn MCMV persistent infection, when MCMV was detected only in the salivary gland, T cells of mice were modified to produce a massive amount of such cytokines as TNF-alpha and IFN-gamma upon in vivo stimulation with anti-CD3.
Rajan et al. (2000)TNF-alphaT cellsPreviously, we showed that depletion of gamma delta T cells significantly reduced clinical and pathological signs of disease, which was associated with reduced expression of IL-1 beta, IL-6, TNF-alpha, and lymphotoxin at disease onset and a more persistent reduction in IFN-gamma.
Kjaergaard et al. (2000)tumor necrosis factorT cellsThe OX-40 receptor (OX-40R) is a cell surface glycoprotein of the tumor necrosis factor receptor family that is expressed primarily on activated CD4 T cells.
Fujiki et al. (1999)tumor necrosis factorT cellsThe expressions of tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, JE/monocyte chemoattractant protein-1, regulated on activation, normal T cells expressed and secreted, and KC/gro messenger RNA (mRNA) in BALF cells from SEB-treated mice peaked at Day 3.
Suzuki et al. (1999)tumor necrosis factorT cellsIL-2Rbeta(1/+) T cells that eliminated activated IL-2Rbeta(2/-) T cells expressed FasL, perforin, granzyme B, and tumor necrosis factor alpha/beta.
Del Sero et al. (1999)TNF-alphaT cellsThe increased resistance to infections as compared to wild-type mice was associated with upregulation of innate and acquired antifungal Th1 responses, such as a dramatically higher production of IL-12, nitric oxide (NO) and TNF-alpha as well as IFN-gamma by CD4+ T cells.
Mu and Thoman (1999)tumor necrosis factorT cellsCytokine production by aged CD8+ T cells differs from that by CD8+ T cells derived from young animals in that a significantly higher percentage of the aged can be triggered to produce interleukin (IL)-4, interferon (IFN)-gamma, and tumor necrosis factor alpha (TNF alpha).
Wei et al. (1999)TNF-alphaT cellThis was accompanied by a reduction in the levels of Ag-induced splenic T cell proliferation, decreased IFN-gamma and TNF-alpha synthesis, but increased IL-4 production by the mutant mice compared with the wild-type mice.
Cope et al. (1999)tumor necrosis factorT cellsDRalphabeta1*0401-restricted, antigen-specific T cells produced significantly more interferon-gamma and tumor necrosis factor a in response to HCgp-39 than did T cells from DRalphabeta1*0402 transgenic mice.
DeBenedette et al. (1999)TNFT cells4-1BB ligand (4-1BBL) is a member of the TNF family expressed on activated APC. 4-1BBL binds to 4-1BB (CD137) on activated CD4 and CD8 T cells and in conjunction with strong signals through the TCR provides a CD28-independent costimulatory signal leading to high level IL-2 production by primary resting T cells.
Bettelli et al. (1998)TNF-alphaT cellsT cells from IL-10(-/-) mice exhibit a stronger Ag-specific proliferation, produce more proinflammatory cytokines (IFN-gamma and TNF-alpha) when stimulated with an encephalitogenic peptide, and induce very severe EAE upon transfer into wild-type mice.
Allen et al. (1993)tumor necrosis factorT cellsThe results reported here indicate that a wide range of cytokines, including interleukin (IL)-4, IL-10, interferon-gamma, tumor necrosis factor beta and macrophage inflammatory protein-1 alpha, are indeed differentially expressed in acute and chronic GVHD and support the concept that the pathology peculiar to acute or chronic GVHD may arise due to differential cytokine expression by activated T cells.
Probert et al. (1993)tumor necrosis factorT cellWasting, ischemia, and lymphoid abnormalities in mice expressing T cell-targeted human tumor necrosis factor transgenes.
Voskuhl et al. (1993)tumor necrosis factorT cellIn the current report, human T cell lines specific for an immunodominant region of MBP were shown to have a functional phenotype similar to T helper 1 (Th1) inflammatory cells of the mouse on the basis of their antigen-specific cytotoxic activity and production of interferon-gamma and lymphotoxin/tumor necrosis factor-alpha, but not interleukin-4.
Mizoguchi et al. (1992)tumor necrosis factorT cellsIn an in vivo murine colon carcinoma model (MCA-38), animals bearing a tumor longer than 26 days develop CD8+ T cells with impaired cytotoxic function, decreased expression of the tumor necrosis factor-alpha and granzyme B genes, and decreased ability to mediate an antitumor response in vivo.
Murray et al. (1990)TNFT cellCells of the expanded abnormal T cell subset were shown to express genes encoding interferon (IFN)-gamma, tumor necrosis factor (TNF)-beta, TNF-alpha and interleukin (IL)6, cytokines which are associated with inflammatory immune responses.