Relevant bibliographies by topics / Tumor necrosis factor alpha (TNFalpha)

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  2. Dissertations / Theses
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Academic literature on the topic 'Tumor necrosis factor alpha (TNFalpha)'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Tumor necrosis factor alpha (TNFalpha)"

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Benbrahim-Tallaa, L., F. Boussouar, C. Rey, and M. Benahmed. "Tumor necrosis factor-alpha inhibits glutathione S-transferase-alpha expression in cultured porcine Sertoli cells." Journal of Endocrinology 175, no. 3 (December 1, 2002): 803–12. http://dx.doi.org/10.1677/joe.0.1750803.

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Glutathione S-transferases (GSTs) are a family of soluble enzymes of detoxification that use reduced glutathione in conjugation and reduction reactions. Toxic electrophiles are substrates for the GSTs. GSTalpha is expressed at high levels in different tIssues such as the testis. Among the different GSTs present in the testis, GSTalpha is specifically expressed in Leydig and Sertoli cells known to be under the control of hormonal and local regulatory factors. The present study investigated the regulatory action of tumor necrosis factor-alpha (TNFalpha) on basal and hormone (FSH and testosterone)-stimulated GSTalpha expression in cultured Sertoli cells. Treatment with TNFalpha (0-20 ng/ml, 48 h) induced a decrease in basal GSTalpha mRNA levels in a dose-dependent manner (fivefold decrease; P<0.001). The maximal and half maximal effects were observed at 20 ng/ml and 7 ng/ml respectively. The inhibitory effect of TNFalpha was also time-dependent with a maximal inhibitory effect (threefold decrease; P<0.001) observed at 48 h. The inhibitory effect of the cytokine was also observed on basal GSTalpha protein (28 kDa) levels. TNFalpha also inhibited the hormone-stimulated GSTalpha expression in Sertoli cells. The treatment of cultured Sertoli cells with both FSH and TNFalpha (100 ng/ml and 10 ng/ml respectively, 48 h) resulted in a complete suppression of the stimulatory action of FSH on GSTalpha mRNA levels. Similarly, in Sertoli cells treated with testosterone or its non-aromatizable metabolite dihydrotestosterone (100 ng/ml, 24 h), TNFalpha reduced the hormone-stimulated GSTalpha mRNA and protein levels. TNFalpha inhibited basal GSTalpha expression without affecting mRNA stability. Indeed, the decay curves (mRNA half-life time=18 h) for the GSTalpha basal mRNA levels in Sertoli cells was similar in the absence or presence of TNFalpha (10 ng/ml, 48 h). Testosterone increased GSTalpha mRNA without affecting the enzyme mRNA stability. TNFalpha antagonized the androgen-stimulated GSTalpha mRNA levels without affecting the enzyme mRNA stability, suggesting that the interaction between the androgen and the cytokine is mostly exerted at a transcriptional level. FSH increased GSTalpha mRNA levels through an increase in mRNA stability (increased mRNA half-life times to 119 h). TNFalpha antagonized the stimulatory effect of FSH on GSTalpha mRNA levels by antagonizing the stabilizing effect exerted by the hormone on GSTalpha mRNA. Together, these results suggest that the increase in the cytokine levels within the testis would alter the detoxification processes against genotoxic products during spermatogenesis.
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Warne, JP. "Tumour necrosis factor alpha: a key regulator of adipose tissue mass." Journal of Endocrinology 177, no. 3 (June 1, 2003): 351–55. http://dx.doi.org/10.1677/joe.0.1770351.

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In addition to its established role in the immune system, tumour necrosis factor alpha (TNFalpha) exerts complex regulatory actions on adipose tissue. TNFalpha is produced in and secreted by the adipocyte and thus is in a position to exert a paracrine and/or autocrine role within adipose tissue. TNFalpha affects many aspects of adipocyte function, from adipocyte development to lipid metabolism. Bringing together all of these diverse actions, TNFalpha appears to play a general role in reducing adipose tissue mass. Dysregulation of TNFalpha production and/or action could be one facet in the development of cachexia and obesity, as well as associated metabolic disorders such as insulin resistance.
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Brotas, Arles Martins, José Marcos Tellas Cunha, Eduardo Henrique Jorge Lago, Cristiane Chaves Nascentes Machado, and Sueli Coelho da Silva Carneiro. "Tumor necrosis factor-alpha and the cytokine network in psoriasis." Anais Brasileiros de Dermatologia 87, no. 5 (October 2012): 673–83. http://dx.doi.org/10.1590/s0365-05962012000500001.

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New molecular methods of research have greatly expanded the knowledge about the role of cytokines in several diseases, including psoriasis. The work orchestrated by these peptides is essential for the communication between resident inflammatory cells (keratinocytes and endothelial cells) and infiltrating cells (neutrophils, lymphocytes, Langerhans cells). This is a complex network due to redundancy, synergism and, sometimes, the antagonism of cytokines, which prevents full understanding of the pathogenesis of the disease. Currently, it seems premature to try to establish a main actor, but TNFalpha participates in all stages of psoriatic plaque development, as we shall see.
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Schmitz, H., M. Fromm, C. J. Bentzel, P. Scholz, K. Detjen, J. Mankertz, H. Bode, H. J. Epple, E. O. Riecken, and J. D. Schulzke. "Tumor necrosis factor-alpha (TNFalpha) regulates the epithelial barrier in the human intestinal cell line HT-29/B6." Journal of Cell Science 112, no. 1 (January 1, 1999): 137–46. http://dx.doi.org/10.1242/jcs.112.1.137.

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Cytokines are supposed to be mediators in diarrhoeal diseases. The aim of this study is to characterize the effect of tumor necrosis factor-alpha (TNFalpha) on epithelial barrier function in the colonic epithelial cell line HT-29/B6. Active ion transport and barrier function were measured as short-circuit current and transepithelial electrical resistance (Rt), respectively. In parallel, freeze-fracture electron microscopy (EM) of tight junctions (TJ) and immunofluorescence microscopy of the zonula occludens protein-1 (ZO-1) were performed. Serosal addition of TNF(alpha) (100 ng/ml) decreased Rt by 81%. This effect was dose-dependent and could be mimicked by antibodies against the p55 form of the TNF receptor. Cytotoxic effects were excluded by a negative lactate dehydrogenase (LDH) assay. Immunofluorescence localization with anti-ZO-1 antibodies revealed no evidence for disruption of the monolayer after TNFalpha treatment. In freeze-fracture EM, TJ complexity was decreased by TNFalpha, as indicated by a decrease in the number of strands from 4.7 to 3.4. The tyrosine kinase blocker genistein and the protein kinase A inhibitor H-8 reduced the effect of TNFalpha. A combination of TNFalpha with interferon-gamma acted synergistically on the epithelial barrier. In conclusion, TNFalpha impairs epithelial barrier function by altering structure and function of the tight junction, which could be of pathogenic relevance in intestinal inflammation.
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5

Nestor, Avgoustidis, Sipsas Nikolaos, Evangelou Konstantinos, and Pikazis Dimitrios. "Tuberculous bursitis of the wrist after anti-TNFalpha treatment: a case report." Open Medicine 5, no. 1 (February 1, 2010): 62–64. http://dx.doi.org/10.2478/s11536-009-0078-6.

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AbstractIn this report, we describe a case of tuberculous bursitis-osteomyelitis of the wrist, in an elderly patient with rheumatoid arthritis and anti-TNFalpha (anti-Tumor Necrosis Factor alpha) treatment.
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6

Gillio Tos, A., A. Cignetti, G. Rovera, and R. Foa. "Retroviral vector-mediated transfer of the tumor necrosis factor alpha gene into human cancer cells restores an apoptotic cell death program and induces a bystander-killing effect." Blood 87, no. 6 (March 15, 1996): 2486–95. http://dx.doi.org/10.1182/blood.v87.6.2486.bloodjournal8762486.

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Tumor necrosis factor alpha (TNFalpha) may induce tumor cell death by apoptosis, the physiologic program of cell death usually lost during neoplastic progression. However, many tumor cells are resistant to its effect unless high doses are administered. By retroviral vector- mediated gene transfer, we have transduced the TNFalpha gene into the DNA of human tumor cells to investigate whether the indefinite neoplastic cell proliferation could be blocked and the lost physiologic program of cell death restored. Evidence is provided that high-TNFalpha- producing clones generated from a human lymphoma T-cell line (ST4) can undergo apoptosis following transduction of the TNFalpha gene. Internucleosomal DNA cleavage was documented by May-Grunwald-Giemsa and by propidium iodide staining, as well as by gel electrophoresis. The induced apoptotic phenomenon is TNFalpha-mediated, since it can be reverted following incubation with anti-TNFalpha monoclonal antibodies (MoAbs), and it occurs with cytokine levels released in the supernatant by the engineered cells much lower(>100 times) than those required to promote the same effect on parental ST4 cells following administration of exogenous recombinant TNFalpha. The process is associated with a downregulation of the apoptosis-preventing gene, bcl-2, while the expression of bax and p53, genes usually involved in promoting apoptosis, persists. Mixed-culture experiments performed coincubating TNFalpha-transduced and untransduced ST4 cells allowed documentation of a bystander-killing effect on the parental cells. This phenomenon still occurred at transduced to parental cell ratios as low as 1:20 and was blocked in the presence of an anti-TNFalpha MoAb. These findings indicated that TNFalpha may play a regulatory role in the proliferation of human tumor cells, and suggest potential new antitumor therapeutic strategies based on the direct delivery of the TNFalpha gene into cancer cells.
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Caux, C., B. Vanbervliet, C. Massacrier, I. Durand, and J. Banchereau. "Interleukin-3 cooperates with tumor necrosis factor alpha for the development of human dendritic/Langerhans cells from cord blood CD34+ hematopoietic progenitor cells." Blood 87, no. 6 (March 15, 1996): 2376–85. http://dx.doi.org/10.1182/blood.v87.6.2376.bloodjournal8762376.

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We have previously shown that tumor necrosis factor (TNF)alpha strongly potentiates the granulocyte-macrophage colony-stimulating factor (GM- CSF)/interleukin (IL)-3-dependent proliferation of CD34+ hematopoietic progenitor cells (HPC) through the recruitment of early progenitors with high proliferative potential. Furthermore, the combination of GM- CSF and TNFalpha allows the generation of large numbers of dendritic/Langerhans cells (D-Lc). Herein, we analyzed whether IL-3, when combined to TNFalpha would, as does GM-CSF, allow the generation of CD1a+ D-Lc. Accordingly, cultures of cord blood CD34+ HPC with IL-3 + TNFalpha yielded 20% to 60% CD14+ cells and 11% to 17% CD1a+ cells, while IL-3 alone did not generate significant numbers of CD1a+ cells. Although the percentage of CD1a+ cells detected in IL3 + TNFalpha was lower than that observed in GM-CSF + TNFalpha (42% to 78%), the strong growth induced by IL-3 + TNFalpha generated as many CD1a+ cells as did GM-CSF + TNFalpha. The CD14+ and CD1a+ cells generated with IL-3 + TNFalpha are similar to CD14+ and CD1a+ cells generated in GM-CSF alone and GM-CSF + TNFalpha, respectively. CD1a+ cells differed from CD14+ cells by (1) dendritic morphology, (2) higher expression of CD1a, CD1c, CD4, CD40, adhesion molecules (CD11c, CD54, CD58), major histocompatibility complex (MHC) class II molecules and CD28 ligands (CD80 and CD86), (3) lack of Fc receptor FcgammaRI (CD64) and complement receptor CR1 (CD35) expression, and (4) stronger induction of allogeneic T-cell proliferation. Thus, in combination with TNFalpha, IL-3 is as potent as GM-CSF for the generation of CD1a+ D-Lc from cord blood CD34+ HPC. The dendritic cell inducing ability of IL-3 may explain why mice with inactivated GM-CSF gene display dendritic cells.
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Jia, L., SM Kelsey, MF Grahn, XR Jiang, and AC Newland. "Increased activity and sensitivity of mitochondrial respiratory enzymes to tumor necrosis factor alpha-mediated inhibition is associated with increased cytotoxicity in drug-resistant leukemic cell lines." Blood 87, no. 6 (March 15, 1996): 2401–10. http://dx.doi.org/10.1182/blood.v87.6.2401.bloodjournal8762401.

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The drug-resistant leukemic cell lines, CEM/VLB100 and K/DAU600, are more sensitive to tumor necrosis factor alpha (TNFalpha)-mediated cytotoxicity compared with their parental cell lines, CCRF-CEM and K562 cl.6. Drug-resistant leukemic cell lines have more active mitochondrial function, which is associated with a greater susceptibility to TNFalpha- induced respiratory inhibition. TNFalpha blocked electron transfer at three sites, NADH dehydrogenase (complex I), succinate dehydrogenase (complex II), and cytochrome c oxidase (complex IV). Respiratory rate and electron transport chain enzyme activities were significantly inhibited in the drug-resistant, TNF-sensitive cell lines. Respiratory inhibition preceded cell death by at least 5 to 8 hours. The respiratory failure was not compensated for by appropriate up- regulation of the glycolytic pathway. Increasing mitochondrial respiratory rate and enzyme activities by long-term culture with 2 mmol/L adenosine 5′-diphosphate (ADP) and Pi sensitized both drug- sensitive and drug-resistant cells to TNFalpha-induced cytolysis. Intramitochondrial free radicals generated by paraquat only had a limited and delayed effect on respiratory inhibition and cytolysis in comparison with the effect of TNFalpha. We conclude that TNFalpha- induced cytotoxicity in leukemic cells is, at least in part, mediated by inhibition of mitochondrial respiration. Free radical generation by TNFalpha may not directly lead to the observed inhibition of the mitochondrial electron transport and other mechanisms must be involved.
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Fasshauer, M., J. Klein, S. Krahlisch, U. Lossner, M. Klier, M. Bluher, and R. Paschke. "GH is a positive regulator of tumor necrosis factor alpha-induced adipose related protein in 3T3-L1 adipocytes." Journal of Endocrinology 178, no. 3 (September 1, 2003): 523–31. http://dx.doi.org/10.1677/joe.0.1780523.

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Tumor necrosis factor (TNF) alpha-induced adipose-related protein (TIARP) has recently been cloned as a TNFalpha-stimulated protein expressed in adipocytes. Its expression is differentiation-dependent and potentially involved in mediating TNFalpha-induced insulin resistance. To further characterize regulation of TIARP gene expression, 3T3-L1 adipocytes were treated with key hormones modulating insulin sensitivity and influencing adipocyte metabolism, and TIARP gene expression was determined by quantitative real-time RT-PCR. Interestingly, TIARP mRNA expression was stimulated almost 9-fold after 500 ng/ml GH were added for 16 h whereas addition of 10 microM isoproterenol, 100 nM insulin and 100 nM dexamethasone for 16 h significantly decreased TIARP gene expression to between 35 and 50% of control levels. In contrast, angiotensin 2 (10 microM) and triiodothyronine (1 microM) did not have any effect. The stimulatory effect of GH was time- and dose-dependent with stimulation occurring as early as 1 h after effector addition and at concentrations as low as 5 ng/ml GH. Moreover, pharmacological inhibition of Janus kinase 2 and p42/44 mitogen-activated protein kinase reversed the stimulatory effect of GH, suggesting that both signaling molecules are involved in activation of TIARP gene expression by GH. Furthermore, an increase of TIARP mRNA could be completely reversed to control levels by withdrawal of GH for 24 h. Taken together, these results show that TIARP is not only responsive to TNFalpha but also to important other hormones influencing glucose homeostasis and adipocyte metabolism. Thus, this factor may play an integrative role in the pathogenesis of insulin resistance and its link to obesity.
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Lambert, GL, S. Barker, DM Lees, and R. Corder. "Endothelin-2 synthesis is stimulated by the type-1 tumour necrosis factor receptor and cAMP: comparison with endothelin-converting enzyme-1 expression." Journal of Molecular Endocrinology 24, no. 2 (April 1, 2000): 273–83. http://dx.doi.org/10.1677/jme.0.0240273.

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ABSTRACT The synthesis of the vasoconstrictor peptide endothelin-2 (ET-2) is dependent on hydrolysis of the biologically inactive intermediate big ET-2 by an endothelin-converting enzyme (ECE). Here, mechanisms inducing ET-2 synthesis have been investigated using the human renal adenocarcinoma cell line (ACHN). Synthesis of ET-2 by ACHN cells was inhibited by phosphoramidon (IC(50( congruent with11 microM). To determine whether ET-2 synthesis occurs in parallel with the metallopeptidase ECE-1, a putative processing peptidase for big ET-2, changes in the levels of their mRNAs were compared by semi-quantitative RT-PCR under conditions causing the upregulation of ET-2 synthesis. Tumour necrosis factor-alpha (TNFalpha), forskolin and a cell-permeable cAMP analogue (dibutyryl cAMP) caused concentration-dependent increases in ET-2 synthesis. Combination of forskolin or dibutyryl cAMP with TNFalpha produced a significantly greater increase in ET-2 production than these agents alone, indicating that adenylate cyclase and TNFalpha induce ET-2 synthesis by separate signalling pathways. Studies using receptor selective TNFalpha mutants, (125(I-TNFalpha binding and TNF receptor mRNA showed that type-1 TNF receptors mediate the ET-2 response to TNFalpha. PreproET-2 mRNA levels were increased by TNFalpha at 1 h and 2 h, but returned to control levels at 4 h. Treatment with forskolin significantly increased preproET-2 mRNA levels after 1 h and 4 h. ACHN cells expressed ECE-1b and ECE-1c, but not the ECE-1a isoform of this peptidase. RT-PCR for the combined isoforms ECE-1b/c/d showed TNFalpha to increase mRNA levels at 2 h and 4 h. Forskolin had no effect on ECE-1b/c/d mRNA levels. Thus, expression of ET-2 and ECE-1b/c/d mRNAs in ACHN cells do not display the co-ordinated regulation observed with typical peptide prohormone processing enzymes and their substrates.
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Dissertations / Theses on the topic "Tumor necrosis factor alpha (TNFalpha)"

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Dinnetz, Joyce Marie. "Omega-3 fatty acid supplementation reduces basal TNFalpha but not toll-like receptor stimulated TNFalpha in full sized and miniature mares." Thesis, Manhattan, Kan. : Kansas State University, 2009. http://hdl.handle.net/2097/1497.

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Beck, Eichler-Jonsson Claudia. "Aspects of mitogen-activated protein kinase cascade activation by epidermal growth factor (EGF): kinetics and crosstalk mechanism with tumor necrosis factor Alpha (TNFalpha) /." [S.l. : s.n.], 2002. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10252924.

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Derouich-Guergour, Dorra. "Etude de la régulation de l'expression des récepteurs du Tumor Necrosis Factor alpha (TNFalpha) au cours de l'infection par Toxoplasma gondii (modèle humain in vitro)." Université Joseph Fourier (Grenoble), 2001. http://www.theses.fr/2001GRE10162.

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Toxoplasma gondii est un protozoaire opportuniste responsable de la toxoplasmose, affection pouvant entraîner des atteintes cliniques graves chez les immunodéprimés et en cas d'atteintes congénitales. Le TNF[alpha], cytokine pro-inflammatoire, a une importance primordiale dans le contrôle de l'infection toxoplasmique. Elle agit par l'intermédiaire de deux récepteurs membranaires :TNFR1 et TNFR2. Nous avons étudié l'expression des récepteurs du TNF[alpha] au cours de l'infection de cellules humaines fibroblastiques MRC5 et de cellules myélomonocutaires THP-1 par T. Gondii. La modulation des TNFRs PAR T. Gondii, in vitro, semble dépendre du type cellulaire utilisé. Nos résultats indiquent que l'infection de cellules d'origine macrophagique (THP-1) par les tachyzoi͏̈tes de la souche RH de T. Gondii est responsable d'une baisse des TNFRs membranaires associée à une augmentation de la libération de TNFR1 solubles dans le milieu de culture. Nous montrons également qu'une pénétration active des parasites est nécessaire et que certains antigènes parasitaires thermosensibles semblent être impliqués. Ce mécanisme de régulation des TNFRs pourrait influencer le rôle du TNF[alpha] dans la toxoplasmose. En effet, ces formes solubles produites par clivage protéolytique des récepteurs membranaires sont capables de se fixer au TNF[alpha] et de réguler sa bio-activité.
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Molgat, André. "The Effect of Macrophage-secreted Factors on Preadipocyte Survival." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23628.

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Adipose tissue (AT) expansion and remodeling that maintains healthy function relies on stromal preadipocytes capable of differentiating into new adipocytes (adipogenesis). During chronic positive energy balance, a relative deficit in adipogenesis, from either a decrease in preadipocyte number or their capacity to differentiate, leads to excessive adipocyte hypertrophy and AT dysfunction. AT contains macrophages whose number and activation state is dynamically regulated with changes in AT mass. This study aims to investigate the effect of macrophage-secreted factors on preadipocyte survival. To assess the effect of macrophage-secreted factors on preadipocytes, murine 3T3-L1 preadipocytes or human primary preadipocytes were incubated with macrophage-conditioned medium (MacCM), prepared from either murine (J774A.1, RAW264.7, bone marrow-derived) or human (THP-1, monocyte-derived) macrophage models, respectively. MacCM inhibited preadipocyte apoptosis and activated pro-survival signaling in both preadipocyte models. Inhibition of PDGFR, Akt, or ERK1/2 reduced the pro-survival effect of MacCM in 3T3-L1 preadipocytes. Inhibition of reactive oxygen species (ROS) generation, or enhancement of ROS clearance, reduced MacCM-dependent 3T3-L1 preadipocyte survival. Whereas anti-inflammatory activated macrophages retained the ability to prevent preadipocyte apoptosis, pro-inflammatory activated macrophages did not. TNF-α immunoneutralization restored the survival activity of pro-inflammatory MacCM on 3T3-L1 preadipocytes. These studies reveal a novel pro-survival effect of MacCM on preadipocytes, and identify signaling molecules (PDGF, Akt, ERK1/2, and ROS) that underlie this action. Macrophage activation was found to regulate the pro-survival activity of MacCM. These in vitro cell culture studies are consistent with a model in which the extent of preadipocyte apoptosis in vivo may determine preadipocyte number and the ability of AT to expand while maintaining healthy function during chronic positive energy balance.
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Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /." Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.

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Watts, Alan D. "The biological role of transmembrane tumour necrosis factor [alpha]." Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27668.

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Tumour necrosis factor (TNF) exists in two physiological forms. One is a soluble polypeptide of 17 kDa, and the other a type II integral membrane protein of 26 kDa designated transmembrane TNF. Soluble TNF is derived from the transmembrane form by proteolytic processing. The soluble TNF molecule exerts potent cytotoxic activity against certain types of cancer cells, and plays a critical role in the functioning of the immune and inflammatory system. The transmembrane TNF molecule shares many of the properties of the soluble form in vitro, but its function in the immune system is not as clearly defined as for the sTNF form. In this thesis the biological role of transmembrane TNF was investigated. The synthesis and expression of both soluble TNF and transmembrane TNF forms was examined in macrophage cells stimulated with LPS. Basic parameters for the production of transmembrane TNF were established to enable further analysis of its function. Using a hydroxamic acid-based inhibitor of TNF processing it was possible to obtain macrophage cells that expressed transmembrane TNF, but not soluble TNF; This enabled the investigation of transmembrane TNF free from the complicating effects of soluble TNF. It was found that inhibition of TNF processing in this way caused an accumulation of transmembrane TNF on the macrophage cells surface 5.1-7.5-fold greater than in cells not treated with the hydroxamic acid-based inhibitor. This corresponded to a 6.4-fold increase in TNF-mediated cytotoxicity of macrophage cells towards cells sensitive to transmembrane TNF. By radiolabelling macrophages, and using a specialised immunoprecipitation method, it was demonstrated that a soluble form of one of the TNF receptors (sTNFFi) binds transmembrane TNF. The consequence of this binding was neutralisation of transmembrane TNF-mediated cytotoxicity, but not inhibition of proteolytic processing of transmembrane TNF to release soluble TNF. The possibility that transmembrane TNF is capable of transducing a signal upon ligation with sTNFR was investigated. A broad range of cellular parameters were measured to see whether sTNFFi treatment of macrophages expressing transmembrane TNF induced a biochemical/physiochemical change. It was found that sTNFR caused a large increase (~200%) in ix intracellular calcium levels after 15 min treatment. This is the first direct evidence that transmembrane TNF is capable of acting like a receptor. The composition of the predicted amino acid sequence of transmembrane TNF was closely examined to determine the presence of features important for both structure and intracellular signalling. A model is presented in Chapter 6 which outlines in diagrammatic form likely structural features of transmembrane TNF. The molecule is predicted to possess a region of cytoplasmic alpha-helices corresponding to a highly conserved domain of the sequence. The structure of transmembrane TNF is consistent with that of a transmembrane receptor, capable of transducing signals initiated by ligation with an extracellular ligand. The comparison of predicted amino acid sequences of transmembrane TNF from different mammalian species revealed the presence of a conserved casein kinase | site. This site was also found to be present in most members of the TNF ligand family. Using orthophosphate labelling, it was shown that mouse transmembrane TNF is phosphorylated in macrophages. Ligation of sTNFR with transmembrane TNF induced de-phosphorylation of mTNF. This de-phosphorylation could be prevented by pre-incubation of the cells with serine phosphatase inhibitors. A selective inhibitor of casein kinase | dramatically reduced the phosphorylation of transmembrane TNF produced by macrophages. In addition, a recombinant form of casein kinase l phosphorylated transmembrane TNF in vitro on the site naturally phosphorylated by the endogenous kinase in vivo. The evidence presented in this study supports an entirely new role for transmembrane TNF, one in which the molecule is capable of acting like a transmembrane receptor, with the ligand being sTNFR. This phenomenon is known as "reverse signalling", and has been shown by other researchers to occur in the majority of members of the TNF ligand family. Implications of mTNF "reverse signalling" are relevant to the treatment of human diseases in which sTNFRs are currently being assessed in clinical trials.
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Nguyen, Thanh Minh. "Tumor necrosis factor alpha (TNF-[alpha]) signal transduction pathways in cyclooxygenase-2 expression /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486459267519688.

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Babu, Kesavan Suresh. "The role of tumor necrosis factor alpha (TNF-α) in asthma." Thesis, University of Southampton, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439378.

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Bond, Arden Lenore. "The production and characterization of a putative anti-idiotypic antibody to tumor necrosis factor-[alpha] /." This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-05042010-020132/.

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Hurst, Liam Andrew. "The role of tumour necrosis factor alpha in pulmonary arterial hypertension." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648471.

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Books on the topic "Tumor necrosis factor alpha (TNFalpha)"

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Friedman, Sonia. The roles of lymphotoxin and tumor necrosis factor-alpha in the pathogenesis of experimental allergic encephalomyelitis. [New Haven, Conn: s.n.], 1993.

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International Conference on Tumor Necrosis Factor and Related Cytokines (4th 1992 Veldhoven, Netherlands). Tumor necrosis factor: Molecular and cellular biology and clinical relevance. Edited by Fiers Walter and Buurman Wim A. Basel: Karger, 1993.

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Bruce, Beutler, ed. Tumor necrosis factors: The molecules and their emerging role in medicine. New York: Raven Press, 1992.

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T, Osawa, and Bonavida Benjamin, eds. Tumor necrosis factor: Structure-function relationship and clinical application. Basel: Karger, 1992.

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Cournoyer, Micheline. Circulating endotoxin, interleukin-6 and tumor necrosis factor alpha in a porcine model of intraabdominal sepsis. Ottawa: National Library of Canada, 1995.

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Moldoveanu, Andrei Ion. Effects of prolonged endurance exercise on the gene expression and plasma levels of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. Ottawa: National Library of Canada, 1999.

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Marialuisa, Melli, and Parente Luca, eds. Cytokines and lipocortins in inflammation and differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of IL-1, TNF, and Lipocortins in Inflammation and Differentiation, held in Siena, Italy, October 22-25, 1989. New York, NY: Wiley-Liss, 1990.

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International Symposium on Artificial Organs, Biomedical Engineering, and Transplantation (1986 Salt Lake City, Utah). Artificial organs: Proceedings of the International Symposium on Artificial Organs, Biomedical Engineering, and Transplantation in honor of the 75th Birthday of Willem J. Kolff. New York, NY: VCH, 1987.

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Dworkin, Chaim R. The use of growth factors in cancer therapy. [Bethesda, Md.?]: U.S. DHHS, PHS, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1993.

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L, Moses Harold, Lengyel Peter 1929-, Stiles Charles D, and Genentech Inc, eds. Growth inhibitory and cytotoxic polypeptides ; proceedings of a Genentech-Smith, Kline & French-Triton Biosciences-UCLA Symposium held in Keystone, Colorado, January 24-30, 1988. New York: A.R. Liss, 1989.

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Book chapters on the topic "Tumor necrosis factor alpha (TNFalpha)"

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Wallach, David, and Andrew Kovalenko. "Tumor Necrosis Factor Alpha (TNFalpha)." In Compendium of Inflammatory Diseases, 1273–82. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_38.

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Wallach, David, and Andrew Kovalenko. "Tumor Necrosis Factor Alpha (TNFalpha)." In Encyclopedia of Inflammatory Diseases, 1–11. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-0348-0620-6_38-2.

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Brightling, Christopher, Latifa Chachi, Dhan Desai, and Yassine Amrani. "Tumor Necrosis Factor Alpha." In Inflammation and Allergy Drug Design, 225–35. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch18.

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Arampatzis, Adamantios, Lida Mademli, Thomas Reilly, Mike I. Lambert, Laurent Bosquet, Jean-Paul Richalet, Thierry Busso, et al. "Tumor Necrosis Factor Alpha." In Encyclopedia of Exercise Medicine in Health and Disease, 883. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3152.

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Heller, Lois Jane, Celette Sugg Skinner, A. Janet Tomiyama, Elissa S. Epel, Peter A. Hall, Julia Allan, Lara LaCaille, et al. "Tumor Necrosis Factor-Alpha (TNF-Alpha)." In Encyclopedia of Behavioral Medicine, 2009–11. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_72.

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Rohleder, Nicolas. "Tumor Necrosis Factor-Alpha (TNF-Alpha)." In Encyclopedia of Behavioral Medicine, 2280–81. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_72.

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Chua, Joel V., and John W. Baddley. "Anti-tumor Necrosis Factor-Alpha Agents." In Infectious Complications in Biologic and Targeted Therapies, 69–87. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11363-5_5.

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McElroy, Rebecca, Madeleine Ennis, and Bettina C. Schock. "TNFAIP3 (Tumor Necrosis Factor, Alpha-Induced Protein 3)." In Encyclopedia of Signaling Molecules, 5509–16. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101957.

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McElroy, Rebecca, Madeleine Ennis, and Bettina C. Schock. "TNFAIP3 (Tumor Necrosis Factor, Alpha-Induced Protein 3)." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101957-1.

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Bachetti, Tiziana, Angelo Corti, Amerigo Giordano, and Roberto Ferrari. "Tumor Necrosis Factor-Alpha in Chronic Heart Failure." In Developments in Cardiovascular Medicine, 3–8. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2003-0_1.

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Conference papers on the topic "Tumor necrosis factor alpha (TNFalpha)"

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Goel, Raghav, Guilio F. Paciotti, and John C. Bischof. "Tumor necrosis factor-alpha induced enhancement of cryosurgery." In Biomedical Optics (BiOS) 2008, edited by Nikiforos Kollias, Bernard Choi, Haishan Zeng, Reza S. Malek, Brian J. Wong, Justus F. R. Ilgner, Kenton W. Gregory, Guillermo J. Tearney, Henry Hirschberg, and Steen J. Madsen. SPIE, 2008. http://dx.doi.org/10.1117/12.764020.

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Havlucu, Yavuz, Fikret Kurhan, Timur Pirildar, Tugba Goktalay, Aysin Sakar Coskun, Pinar Celik, and Arzu Yorgancioglu. "Pulmonary infections in patients receiving treatment of tumor necrosis factor alpha antagonists." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2647.

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Pereira, Danilo Alves Ponzi, Jessica Batista Lima Logrado, Adinor Junior Diniz Pinheiro, Fabiola Brasil Barbosa Rodrigues, Marilia do Socorro Santos Campos, Glauce Leão Lima, Roberta Vilela Lopes Koyama, Thayana Ribeiro Kajitani Pacheco, Claudia Barros Ohashi, and Gilberto Toshimitsu Yoshikawa. "Leprosy associated with tumor necrosis factor alpha antagonist: report of 3 cases." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.1850.

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Rashad Mahmoud, Alaa, and Asmaa Nafady. "Tumor necrosis factor-alpha and CD4/CD8 ratio in patients with hypersensitivity pneumonitis." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3104.

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Heijink, Anne M., Francien G. Talens, Anouk Baars, and Marcel A. van Vugt. "Abstract 2488: Tumor necrosis factor-alpha signaling determines cytotoxicity induced by BRCA2 deficiency." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2488.

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Gould, Neal S., Elysia Min, and Brian Day. "Utilization Of Extracellular Glutathione By Phagocytosis Reduces Tumor Necrosis Factor Alpha Release In Macrophages." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2808.

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SÁ, MARCUS VILLANDER BARROS DE OLIVEIRA, TAMARA CRISTINA SILVA SOUSA, FRANCISCO BARRETTO, SILVERIO JOSÉ CORREIA CUNHA, and FLAVIO JOSÉ SIQUEIRA PACHECO. "ANTI-TUMOR NECROSIS FACTOR - ALPHA THERAPY IN A PATIENT WITH CD4 LYMPHOPENIC SARCOIDOSIS PHENOTYPE." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-028.

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Polat, Sait. "Expression of Interleukin 6 and Tumor Necrosis Factor Alpha in Endometriotic Tissues: An Immunohistochemical Study." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-166.

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Kim, V., T. Briscoe, N. Thingalaya, GJ Criner, and TJ Rogers. "Interleukin 17 and Tumor Necrosis Factor Alpha Synergistically Increase Muc5AC Expression in Human Airway Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4937.

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Yelnik, CM, L. Gaboriau, N. Petitpain, H. Théophile, C. Scalbert, E. Delaporte, S. Gautier, and M. Lambert. "SAT0144 Tumor necrosis factor-alpha inhibitors and psychiatric side effects: results from the french pharmacovigilance database." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1610.

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Reports on the topic "Tumor necrosis factor alpha (TNFalpha)"

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Tian, Cong, Jianlong Shu, Wenhui Shao, Zhengxin Zhou, Huayang Guo, and Jingang Wang. The efficacy and safety of IL Inhibitors, TNF-α Inhibitors, and JAK Inhibitor on ankylosing spondylitis: A Bayesian network meta-analysis of a “randomized, double-blind, placebo-controlled” trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0117.

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Review question / Objective: In this study, we conducted a Bayesian network meta-analysis to evaluate the efficacy and safety of interleukin (IL) inhibitors, tumor necrosis factor-alpha (TNF-α) inhibitors, and Janus kinase (JAK) inhibitors on ankylosing spondylitis (AS).The purpose of this study is to compare the effectiveness and safety of different interventions for treating AS to provide insights into the decision-making in clinicalpractice. Condition being studied: Ankylosing spondylitis. Based on the Bayesian hierarchical model, we conducted a network meta-analysis using the gemtc package in R software (version 4.1.3) and Stata software (version 15.1). Cong Tian and Jianlong Shu contributed to the conception and design of the study and supervised the tweet classification. All authors drafted the manuscript. Wenhui Shao, Zhengxin Zhou, Huayang Guo and Jingang Wang contributed to data management and tweet classification. Cong Tian, Jianlong Shu and Zhengxin Zhou performed the statistical analysis. Cong Tian, Jianlong Shu, Wenhui Shao and Zhengxin Zhou reviewed the manuscript.
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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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