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TNF, via TNFRp55 signaling, modulates articular progesterone and cytokine circadian rhythms in late pregnancy.
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Recognition memory improved with exercise in WT mice, was impaired in TNFR1(-/-) exercise mice, showed non-significant impairment with exercise in TNF(-/-) mice, and no changes in TNFR2(-/-) mice. In spatial learning there were exercise related improvements in WT mice, non-significant but meaningful impairments evident in TNFR1(-/-) exercise mice, modest improvement in TNF(-/-) exercise mice.
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Transmembrane TNF, TNFR2 and TNFR1 (indirectly) are critical for preventing inflammation during BCG-induced pleurisy in mice.
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Our work suggested that TNF-alpha and TNF-R1 are the major contributors of TNF signaling pathway in anesthesia-induced spinal cord neurotoxicity. Targeting TNF-alpha / TNF-R1, not TNF-R2 signaling pathway may be the key component to rescue or prevent anesthesia-induced apoptotic injury in spinal cord neurons.
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Lack of TNF-alpha signaling through Tnfr1 makes the mice more susceptible to acute infection but does not alter state of latency and reactivation of HSV-1.
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This study demonstrated that the TNFR1, but not TNFR2, is Required for Both Histaminergic and Non-histaminergic Itch in Mice.
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p55TNFR shedding has a prominent role in Th1 mediated protection against chronic and latent tuberculosis infection
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p55TNFR-IKK2-Ripk3 signalling orchestrates arthritogenic and death responses in synovial fibroblasts
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his study shows that CCR-2/TLR-2 triggered signaling in murine peritoneal macrophages intensifies bacterial (Staphylococcus aureus) killing by reactive oxygen species through TNF-R1
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Results provide experimental data on the existence of a TNFRp55-mediated anti-inflammatory circuit in dendritic cells which might contribute to the protection against reactive arthritis during the resolution of Yersinia entercolitica infection.
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TNFR1 contributes to ethanol-induced hypertension and oxidative stress in the vasculature.
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TNFR2 is important for the proliferative expansion of pathogenic Teff cells
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NEMO deficiency hampered activation of IKK complex in osteoclast precursors, causing arrest of osteoclastogenesis and apoptosis. Interestingly, inhibiting apoptosis by genetic ablation of TNFr1 significantly increased cell survival, but failed to rescue osteoclastogenesis or reverse osteopetrosis.
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Data indicate that IL-1RI and TNF-1R contribute to regulation of stress-induced, negatively reinforced drinking perhaps through overlapping signaling events downstream of these receptors, while leaving rewarding properties of alcohol largely unaffected.
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Myeloid-derived suppressor cells from tumor necrosis factor receptor (TNFR) 2(-/-) mice, but not from TNFR1(-/-) mice, failed to promote B-cell responses.
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TNFR2 is required for inflammation-inducible M cells.
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These findings indicate that TNFR1 is structurally positioned to modulate postsynaptic signaling in the PVN, suggesting a mechanism whereby TNFR1 activation contributes to cardiovascular and other autonomic functions.
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Increased TNFR1 expression and signaling in injured peripheral nerves of mice with reduced BACE1 activity
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Results show that interleukin 6 (IL6) promotes oval cell proliferation and liver regeneration, while tumor necrosis factor alpha (TNFalpha) and TNF receptor-1(TNFR1) do not affect this process.
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Data suggest that dietary treatment with green tea extract reduces hepatic inflammation in non-alcoholic fatty liver disease by decreasing proinflammatory signaling in liver through Tnfr1 (tumor necrosis factor receptor superfamily, member 1a) and Tlr4 (toll-like receptor 4) that otherwise increases NFkappaB activation and liver injury.
