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Gene Review

Tnfrsf1b  -  tumor necrosis factor receptor superfamily...

Rattus norvegicus

Synonyms: TNF-R2, TNF-RII, TNFR-II, Tnfr2, Tumor necrosis factor receptor 2, ...
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Disease relevance of Tnfrsf1b


High impact information on Tnfrsf1b

  • Recent studies have demonstrated that neurotrophins may also induce cell death via the p75 receptor [6].
  • These data suggest that the mechanism of apoptosis by NGF through the p75 receptor is different from TNF and Fas-mediated killing. gamma Radiation of oligodendrocytes also activated a similar subset of caspases as NGF, indicating that NGF-induced oligodendrocyte apoptosis uses a similar cell death execution mechanism as injury models [7].
  • Treatment with NGF causes long-term cultures of oligodendrocytes to die via a yet undefined mechanism mediated by the p75 neurotrophin receptor [7].
  • Here, using MRI, we demonstrate that a focal intrastriatal injection of TNF-alpha causes a significant, acute reduction (15-30%) in cerebral blood volume (CBV), which is dependent on TNF-alpha-type 2 receptor (TNFR2) activation, and can be ameliorated by pre-treatment with a non-specific endothelin (ET) receptor antagonist [8].
  • TNF-alpha reduces cerebral blood volume and disrupts tissue homeostasis via an endothelin- and TNFR2-dependent pathway [8].

Biological context of Tnfrsf1b

  • Gene expression of Tnfrsf1a and Tnfrsf1b was downregulated in colon and small intestine of experimental animals, possibly as a mechanism of protection against TNF cytotoxicity [1].
  • In vitro studies showed that pretreatment of naive AM with a TNF-R2 antibody significantly inhibited BLM-induced caspase-3 activity and apoptosis [2].
  • In contrast, TNFR2 expression occurred exclusively on non-neuronal cells of the macrophage-monocyte lineage, with cell numbers increasing in a TNF-dependent fashion during CFA-induced arthritis [5].
  • These data confirm the capacity of TNFR2 to generate an apoptotic cell death signal independent of TNFR1 [9].
  • TRAF2 downregulation, which has been proposed as the mechanism by which TNFR2 enhances TNFR1 signaling, was observed in PC60 cells, but the TNRF1 signal was not modulated [9].

Anatomical context of Tnfrsf1b


Associations of Tnfrsf1b with chemical compounds

  • Methylprednisolone (MP), a synthetic glucocorticoid, partially inhibited the injury-induced expression of TNFR1 and TNFR2, an effect which could be reversed by RU486, an antagonist of glucocorticoid receptors [10].
  • Neurotrophic factors regulate neuronal survival and differentiation and control neurite outgrowth by binding to tyrosine kinase receptors, the Trks, and a tumor necrosis factor (TNF) receptor-like molecule, p75 neurotrophin receptor [14].
  • HSC apoptosis in tissue culture in the presence of serum was quantified after addition of 0.1 to 100 ng/ml of nerve growth factor (NGF) a ligand for p75, by in situ counting of apoptotic bodies after addition of acridine orange [15].
  • In view of the pro-survival roles described for trks and the context-dependent stimulation of survival and cell death pathways activated by p75, differential regulation of these receptors by estrogen is likely to alter neurotrophin-dependent cell signaling [16].
  • Destruction of p75-expressing fibers in the superficial dorsal horn by 192-IgG saporin was not accompanied by changes in acetylcholine or norepinephrine content or by reduction in cholinergic neuronal number in the spinal cord dorsal horn [17].

Other interactions of Tnfrsf1b

  • The temporal pattern of TNFR2 expression was similar to that of TNFR1 but its expression peaked at 4 h postinjury [10].
  • BLM exposure had no marked effect on AM expression of TNF-R1 or caspase-8 activation, but significantly increased the expression of TNF-R2 that was accompanied by a rise in c-IAP1 and a decrease in TRAF2 [2].
  • Receptors mRNAs, except TNF receptor 2 and gp130 mRNAs, showed temporal profiles that were similar to those of their cytokine mRNAs [18].

Analytical, diagnostic and therapeutic context of Tnfrsf1b

  • Using reverse transcription-polymerase chain reaction (RT-PCR) technique, the messenger RNA (mRNA) for tumor necrosis factor receptor type 2 (TNF-R2, 75/80 kDa) was detected in rat primary astrocytes, with much lower level of expression when compared to that for tumor necrosis factor receptor type 1 (TNF-R1, 55/60 kDa) [19].
  • The 55kDa protein of TNFR-1 but not the 75kDa of TNFR-2 was detected by Western blot analysis [20].
  • Using RT-PCR and Northern blotting TNFR1 and TNFR2 mRNAs were found to be constitutively expressed and increased after LPS [21].
  • Surprisingly, we find that a purified preparation of OECs, selected on the basis of low-affinity nerve growth factor receptor (p75) expression, results in less extensive remyelination than an unpurified preparation following transplantation into areas of persistent demyelination in rodent CNS in the X-irradiation/ethidium bromide (X-EB) model [22].
  • In situ hybridization was performed to assess the cellular localization of IGF-1, NGF, p75, and IGF-1R mRNA and immunohistochemistry served to localize the source of p75 and IGF-1R protein expression [23].


  1. Experimental intestinal endometriosis is characterized by increased levels of soluble TNFRSF1B and downregulation of Tnfrsf1a and Tnfrsf1b gene expression. Rojas-Cartagena, C., Appleyard, C.B., Santiago, O.I., Flores, I. Biol. Reprod. (2005) [Pubmed]
  2. Time-dependent apoptosis of alveolar macrophages from rats exposed to bleomycin: involvement of tnf receptor 2. Zhao, H.W., Hu, S.Y., Barger, M.W., Ma, J.K., Castranova, V., Ma, J.Y. J. Toxicol. Environ. Health Part A (2004) [Pubmed]
  3. Pentoxyphilline as a cyclooxygenase (cox-2) inhibitor in experimental sepsis. Modzelewski, B., Janiak, A. Med. Sci. Monit. (2004) [Pubmed]
  4. Cells from newborn rat brain established in primary tissue culture will support rubella virus replication. Van Alstyne, D., Smyrnis, E.M., Singh, V.K. Can. J. Microbiol. (1984) [Pubmed]
  5. The differential contribution of tumour necrosis factor to thermal and mechanical hyperalgesia during chronic inflammation. Inglis, J.J., Nissim, A., Lees, D.M., Hunt, S.P., Chernajovsky, Y., Kidd, B.L. Arthritis Res. Ther. (2005) [Pubmed]
  6. Neurotrophins induce death of hippocampal neurons via the p75 receptor. Friedman, W.J. J. Neurosci. (2000) [Pubmed]
  7. Oligodendrocyte apoptosis mediated by caspase activation. Gu, C., Casaccia-Bonnefil, P., Srinivasan, A., Chao, M.V. J. Neurosci. (1999) [Pubmed]
  8. TNF-alpha reduces cerebral blood volume and disrupts tissue homeostasis via an endothelin- and TNFR2-dependent pathway. Sibson, N.R., Blamire, A.M., Perry, V.H., Gauldie, J., Styles, P., Anthony, D.C. Brain (2002) [Pubmed]
  9. Induction of apoptosis by TNF receptor 2 in a T-cell hybridoma is FADD dependent and blocked by caspase-8 inhibitors. Depuydt, B., van Loo, G., Vandenabeele, P., Declercq, W. J. Cell. Sci. (2005) [Pubmed]
  10. Expression of the type 1 and type 2 receptors for tumor necrosis factor after traumatic spinal cord injury in adult rats. Yan, P., Liu, N., Kim, G.M., Xu, J., Xu, J., Li, Q., Hsu, C.Y., Xu, X.M. Exp. Neurol. (2003) [Pubmed]
  11. Spinal nerve ligation induces transient upregulation of tumor necrosis factor receptors 1 and 2 in injured and adjacent uninjured dorsal root ganglia in the rat. Schäfers, M., Sorkin, L.S., Geis, C., Shubayev, V.I. Neurosci. Lett. (2003) [Pubmed]
  12. Shedding of tumor necrosis factor type 1 receptor after experimental spinal cord injury. Harrington, J.F., Messier, A.A., Levine, A., Szmydynger-Chodobska, J., Chodobski, A. J. Neurotrauma (2005) [Pubmed]
  13. A determination of tumor necrosis factor expression in TMJ inflammation with the use of microarray analysis. Spears, R., Oakes, R., Moore, C., Bellinger, L.L., Hutchins, B. J. Dent. Res. (2003) [Pubmed]
  14. Neurotrophic factors increase tumor necrosis factor-alpha-induced nuclear translocation of NF-kappaB in rat PC12 cells. Furuno, T., Nakanishi, M. Neurosci. Lett. (2006) [Pubmed]
  15. Hepatic stellate cells express the low affinity nerve growth factor receptor p75 and undergo apoptosis in response to nerve growth factor stimulation. Trim, N., Morgan, S., Evans, M., Issa, R., Fine, D., Afford, S., Wilkins, B., Iredale, J. Am. J. Pathol. (2000) [Pubmed]
  16. NGF stimulation increases JNK2 phosphorylation and reduces caspase-3 activity in the olfactory bulb of estrogen-replaced animals. Jezierski, M.K., Sturm, A.K., Scarborough, M.M., Sohrabji, F. Endocrinology (2001) [Pubmed]
  17. P75-expressing elements are necessary for anti-allodynic effects of spinal clonidine and neostigmine. Paqueron, X., Li, X., Eisenach, J.C. Neuroscience (2001) [Pubmed]
  18. Temporal expression of cytokines and their receptors mRNAs in a neuropathic pain model. Lee, H.L., Lee, K.M., Son, S.J., Hwang, S.H., Cho, H.J. Neuroreport (2004) [Pubmed]
  19. Induction of tumor necrosis factor receptor type 2 gene expression by tumor necrosis factor-alpha in rat primary astrocytes. Lung, H.L., Leung, K.N., Stadlin, A., Ma, C.M., Tsang, D. Life Sci. (2001) [Pubmed]
  20. TNF-alpha induces apoptosis of parietal cells. Neu, B., Puschmann, A.J., Mayerhofer, A., Hutzler, P., Grossmann, J., Lippl, F., Schepp, W., Prinz, C. Biochem. Pharmacol. (2003) [Pubmed]
  21. Cell-specific expression and lipopolysaccharide-induced regulation of tumor necrosis factor alpha (TNFalpha) and TNF receptors in rat dorsal root ganglion. Li, Y., Ji, A., Weihe, E., Schäfer, M.K. J. Neurosci. (2004) [Pubmed]
  22. Meningeal cells enhance limited CNS remyelination by transplanted olfactory ensheathing cells. Lakatos, A., Smith, P.M., Barnett, S.C., Franklin, R.J. Brain (2003) [Pubmed]
  23. Early gene responses of trophic factors in nerve regeneration differ in experimental type 1 and type 2 diabetic polyneuropathies. Pierson, C.R., Zhang, W., Murakawa, Y., Sima, A.A. J. Neuropathol. Exp. Neurol. (2002) [Pubmed]
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