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Relevant bibliographies by topics / C57BL/6 TNFR p55 -/- mice

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Academic literature on the topic 'C57BL/6 TNFR p55 -/- mice'

Author: Grafiati

Published: 5 June 2025

Last updated: 1 August 2025

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Journal articles on the topic "C57BL/6 TNFR p55 -/- mice"

1

Huber, S. A., та D. Sartini. "Roles of Tumor Necrosis Factor Alpha (TNF-α) and the p55 TNF Receptor in CD1d Induction and Coxsackievirus B3-Induced Myocarditis". Journal of Virology 79, № 5 (2005): 2659–65. http://dx.doi.org/10.1128/jvi.79.5.2659-2665.2005.

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ABSTRACT Giving C57BL/6 mice 104 PFU of coxsackievirus B3 (H3 variant) fails to induce myocarditis, but increasing the initial virus inoculum to 105 or 106 PFU causes significant cardiac disease. Virus titers in the heart were equivalent at days 3 and 7 in mice given all three virus doses, but day 3 titers in the pancreases of mice inoculated with 104 PFU were reduced. Tumor necrosis factor alpha (TNF-α) concentrations in the heart were increased in all infected mice, but cytokine levels were highest in mice given the larger virus inocula. TNF-α−/− and p55 TNF receptor-negative (TNFR−/−) mice

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2

Bohn, Erwin, Edgar Schmitt, Claudia Bielfeldt, Annette Noll, Ralf Schulte, and Ingo B. Autenrieth. "Ambiguous Role of Interleukin-12 in Yersinia enterocolitica Infection in Susceptible and Resistant Mouse Strains." Infection and Immunity 66, no. 5 (1998): 2213–20. http://dx.doi.org/10.1128/iai.66.5.2213-2220.1998.

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ABSTRACT Endogenous interleukin-12 (IL-12) mediates protection againstYersinia enterocolitica in C57BL/6 mice by triggering gamma interferon (IFN-γ) production in NK and CD4+ T cells. Administration of exogenous IL-12 confers protection against yersiniae in Yersinia-susceptible BALB/c mice but exacerbates yersiniosis in resistant C57BL/6 mice. Therefore, we wanted to dissect the different mechanisms exerted by IL-12 during Yersiniainfections by using different models of Yersinia-resistant and -susceptible mice, including resistant C57BL/6 mice, susceptible BALB/c mice, intermediate-susceptible

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3

Lundberg, Patric, Paula V. Welander, Carl K. Edwards, Nico van Rooijen, and Edouard Cantin. "Tumor Necrosis Factor (TNF) Protects Resistant C57BL/6 Mice against Herpes Simplex Virus-Induced Encephalitis Independently of Signaling via TNF Receptor 1 or 2." Journal of Virology 81, no. 3 (2006): 1451–60. http://dx.doi.org/10.1128/jvi.02243-06.

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ABSTRACT Tumor necrosis factor (TNF) is a multifunctional cytokine that has a role in induction and regulation of host innate and adaptive immune responses. The importance of TNF antiviral mechanisms is reflected by the diverse strategies adopted by different viruses, particularly members of the herpesvirus family, to block TNF responses. TNF binds and signals through two receptors, Tnfrsf1a (TNF receptor 1 [TNFR1], or p55) and Tnfrsf1b (TNFR2, or p75). We report here that herpes simplex virus 1 (HSV-1) infection of TNF−/− mice on the resistant C57BL/6 genetic background results in significant

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4

Pryhuber, Gloria S., David P. O'Brien, Raymond Baggs, et al. "Ablation of tumor necrosis factor receptor type I (p55) alters oxygen-induced lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 5 (2000): L1082—L1090. http://dx.doi.org/10.1152/ajplung.2000.278.5.l1082.

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Hyperoxic lung injury, believed to be mediated by reactive oxygen species, inflammatory cell activation, and release of cytotoxic cytokines, complicates the care of many critically ill patients. The cytokine tumor necrosis factor (TNF)-α is induced in lungs exposed to high concentrations of oxygen; however, its contribution to hyperoxia-induced lung injury remains unclear. Both TNF-α treatment and blockade with anti-TNF antibodies increased survival in mice exposed to hyperoxia. In the current study, to determine if pulmonary oxygen toxicity is dependent on either of the TNF receptors, type I

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5

White, Douglas W., Vladimir P. Badovinac, Xin Fan, and John T. Harty. "Adaptive Immunity against Listeria monocytogenes in the Absence of Type I Tumor Necrosis Factor Receptor p55." Infection and Immunity 68, no. 8 (2000): 4470–76. http://dx.doi.org/10.1128/iai.68.8.4470-4476.2000.

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ABSTRACT Tumor necrosis factor (TNF) and the type I TNF receptor (TNFRI), p55, are critical for resistance against primary infections with the intracellular bacterial pathogen Listeria monocytogenes. Importantly, however, susceptibility to primary listeriosis in cytokine-deficient mice does not preclude the development or expression of effective adaptive immunity against virulent L. monocytogenes. We used TNFRI−/− mice to study adaptive antilisterial immunity in the absence of interactions between TNF and TNFRI. Our experiments indicate that TNFRI−/− mice survive and clear high-dose challenges

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6

Cho, Hye-Youn, Liu-Yi Zhang та Steven R. Kleeberger. "Ozone-induced lung inflammation and hyperreactivity are mediated via tumor necrosis factor-α receptors". American Journal of Physiology-Lung Cellular and Molecular Physiology 280, № 3 (2001): L537—L546. http://dx.doi.org/10.1152/ajplung.2001.280.3.l537.

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This study was designed to investigate the mechanisms through which tumor necrosis factor ( Tnf) modulates ozone (O3)-induced pulmonary injury in susceptible C57BL/6J (B6) mice. B6 [wild-type ( wt)] mice and B6 mice with targeted disruption (knockout) of the genes for the p55 TNF receptor [ TNFR1(−/−)], the p75 TNF receptor [ TNFR2(−/−)], or both receptors [ TNFR1/TNFR2(−/−)] were exposed to 0.3 parts/million O3 for 48 h (subacute), and lung responses were determined by bronchoalveolar lavage. All TNFR(−/−) mice had significantly less O3-induced inflammation and epithelial damage but not lung

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7

Leon, Lisa R., Andrew A. White, and Matthew J. Kluger. "Role of IL-6 and TNF in thermoregulation and survival during sepsis in mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 1 (1998): R269—R277. http://dx.doi.org/10.1152/ajpregu.1998.275.1.r269.

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Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have been implicated as key mediators in inflammation, morbidity, and mortality associated with sepsis. We examined the role of IL-6 and TNF-α signaling on hypothermia, fever, cachexia, anorexia, and survival during sepsis induced by cecal ligation and puncture (CLP) in male and female gene knockout mice. Male wild-type mice developed an initial hypothermia and subsequent fever during sepsis. Male IL-6 knockout mice did not develop fever; rather, they maintained a profound hypothermia during sepsis. Male TNF p55/p75 receptor (TNFR) knock

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8

Haak-Frendscho, M., S. A. Marsters, J. Mordenti, et al. "Inhibition of TNF by a TNF receptor immunoadhesin. Comparison to an anti-TNF monoclonal antibody." Journal of Immunology 152, no. 3 (1994): 1347–53. http://dx.doi.org/10.4049/jimmunol.152.3.1347.

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Abstract TNF is an important mediator of inflammation, which can have deleterious effects when produced inappropriately. We have described a recombinant inhibitor of TNF, termed TNFR-IgG, or TNFR immunoadhesin, composed of the extracellular portion of the type 1 (p55) TNF receptor (TNFR) linked to the hinge and Fc regions of IgG heavy chain. This bivalent, Ab-like molecule is a potent inhibitor of TNF, exhibiting significantly higher affinity for the cytokine than soluble TNFR. Here, we compare the TNF-neutralizing capacity of TNFR-IgG to that of an anti-TNF mAb. In vitro, TNFR-IgG was 10- to

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9

Ehlers, Stefan, Jochen Benini, Stefanie Kutsch, Robert Endres, Ernst T. Rietschel, and Klaus Pfeffer. "Fatal Granuloma Necrosis without Exacerbated Mycobacterial Growth in Tumor Necrosis Factor Receptor p55 Gene-Deficient Mice Intravenously Infected with Mycobacterium avium." Infection and Immunity 67, no. 7 (1999): 3571–79. http://dx.doi.org/10.1128/iai.67.7.3571-3579.1999.

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ABSTRACT The pathogenesis of mycobacterial infections is associated with the formation of granulomas in which both antibacterial protection and tissue damage take place concomitantly. We used murineMycobacterium avium infection to compare the development of granulomatous lesions in intravenously infected tumor necrosis factor receptor p55 (TNFRp55) gene-deficient (p55−/−) mice to the development of granulomatous lesions in M. avium-infected syngeneic C57BL/6 (p55+/+) mice. Up to 5 weeks after infection with either the highly virulent M. avium strain TMC724 or the intermediately virulent M. avi

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10

Zhao, Yi-Xue, Ginette Lajoie, Hongwei Zhang, Basil Chiu, Ursula Payne, and Robert D. Inman. "Tumor Necrosis Factor Receptor p55-Deficient Mice Respond to Acute Yersinia enterocolitica Infection with Less Apoptosis and More Effective Host Resistance." Infection and Immunity 68, no. 3 (2000): 1243–51. http://dx.doi.org/10.1128/iai.68.3.1243-1251.2000.

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ABSTRACT Tumor necrosis factor (TNF) has generally been regarded as a protective cytokine in host defense against bacterial infections. In the present study, we evaluated the role of TNF in the acute phase of infection by Yersinia enterocolitica by using mice rendered genetically deficient in TNF receptor p55 (TNFRp55−/−). Unexpectedly, TNFRp55−/− mice showed more effective resistance to the bacteria, reflected in enhanced bacterial clearance and less tissue damage, than did control C57BL/6 mice. C57BL/6 mice showed evidence of extensive apoptosis in the spleen accompanied by a selective decre

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