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Gene Review

Il1r1  -  interleukin 1 receptor, type I

Rattus norvegicus

Synonyms: CD121 antigen-like family member A, IL-1R-1, IL-1R-alpha, IL-1RT-1, IL-1RT1, ...
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Disease relevance of Il1r1

  • Radioligand binding and electrophoretic mobility shift assays showed that during chronic hypoxia, IL-1 receptor density and activity of the transcription factor NF-kappaB induced by IL-1beta were decreased, which may account at least in part for the decrease in iNOS expression [1].
  • Brain tumor formation was associated with significant increased levels of interleukin (IL)-1beta, IL-1 receptor antagonist, IL-1 receptor type I, tumor necrosis factor (TNF)-alpha, and transforming growth factor (TGF)-beta1 mRNAs in the cerebellum, hippocampus, and hypothalamus [2].
  • In conclusion, this study provides in vivo and in vitro evidence that IL-1 up-regulates OPN expression in experimental kidney disease and support for the argument that inhibition of OPN expression is one mechanism by which IL-1 receptor antagonist treatment suppresses macrophage-mediated renal injury [3].
  • IL-1beta-induced hyperalgesia was blocked by pretreatment with IL-1 receptor antagonist [4].
  • The IL-1 receptor antagonist did not modify MDMA-induced hyperthermia indicating that IL-1beta release is a consequence, not the cause, of the rise in body temperature [5].

High impact information on Il1r1

  • The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets [6].
  • Addition of IL-1 receptor antagonist (RA) eliminated these IL-1 beta effects [7].
  • Conversely, the accumulation of both PAI-1 and collagen induced by IL-1 was inhibited with an IL-1 receptor antagonist (200 ng/mL; n = 6) and with cycloheximide (10 micrograms/mL; n = 6), implying that protein synthesis was a requirement for the effect [8].
  • However, pretreatment with either the IL-1 receptor antagonist or the cyclooxygenase inhibitor flurbiprofen completely abolishes adenovirus-induced fever, suggesting that IL-1 and prostaglandins are direct mediators of this response [9].
  • Specific labeling for mRNAs encoding the type 1 IL-1 receptor and the EP3 subtype of the prostaglandin E2 receptor was detected in situ over neuronal cell bodies in the rat nodose ganglion [10].

Chemical compound and disease context of Il1r1


Biological context of Il1r1


Anatomical context of Il1r1

  • However, only IL-1 receptor antagonist and not an anti-rat TNF-alpha antiserum diminished the extent of iNOS induction in myocytes exposed to this medium and prevented a decline in contractile responsiveness to isoproterenol [17].
  • Moreover, brief applications of IL-1beta to voltage-clamped oocytes yielded a delayed potentiation of the GABA-elicited chloride currents (I(GABA)); this effect was suppressed by IL-1ra, the natural IL-1 receptor (IL-1RI) antagonist [18].
  • AMB-mediated enhancement of astrocyte NO production was partly dependent on endogenous IL-1, as shown by partial inhibition of AMB effect with IL-1 receptor antagonist [19].
  • Additionally, affinity cross-linking studies indicate that the rat brain IL 1 receptor has a m.w. of approximately 80,000, which is similar to the previously described recognition molecule on T cells and fibroblasts [20].
  • We identified the stimulator secreted by macrophages as IL-1 because mesangial cells overexpressing IL-1 receptor antagonist protein showed a blunted expression of MMP-9 in response to the macrophage-conditioned medium [21].

Associations of Il1r1 with chemical compounds


Physical interactions of Il1r1

  • The mechanism by which IL-1 beta exerts its actions in the brain during systemic inflammation is not fully understood, as neither IL-1 receptor gene expression nor IL-1 binding have been identified in significant levels in key areas that respond to IL-1 beta [27].
  • This suggests that dbcAMP-induced synthesis of IL-1beta mediates the C3 production by SchC in an autocrine/paracrine fashion by binding to a functional IL-1 receptor expressed on the surface of SchC [28].
  • Interleukin-1 receptor antagonist (IL-1ra) competes with IL-1 for binding of the IL-1 receptor, but does not elicit a cellular immune response [29].

Regulatory relationships of Il1r1

  • The IL-1RAcp was down-regulated in parallel with the type I IL-1 receptor in the liver following endotoxin treatment in rats [30].
  • These observations suggest that IGF-I may down-regulate ovarian IL-1 action by decreasing type I IL-1R gene expression, while up-regulating sPLA2 gene expression and activity [31].
  • The effect was dependent on time and the dose of IL-1 beta and was blocked by and IL-1 receptor antagonist [32].
  • Moreover, when IL-1 receptor activity was inhibited using an adenoviral vector that expresses the IL-1 receptor antagonist (IL-1ra) in the hippocampus, both short-term and long-term memory retention scores were facilitated [33].
  • Intracerebroventricular, but not iv, administration of 2 micrograms IL-1 receptor antagonist blocked the IL-1 alpha-induced increase [34].

Other interactions of Il1r1

  • RESULTS: Antisense experiment revealed that IL-1R1 was required for iNOS transcription [13].
  • The rat IL-1RAcP has approximately 25% sequence identity to the rat type I IL-1 receptor and a predicted extracellular domain with three immunoglobulin-like loops [30].
  • Treatment with IGF-I resulted in a significant (P< 0.01) decrease in type I IL-1R transcripts (an effect which was reversed by co-treatment with IL-1beta), was without effect on IL-1beta transcripts, and significantly (P < 0.05) increased sPLA2 gene expression (an effect which was further enhanced by co-treatment with IL-1beta) [31].
  • Since phosphorylated ERK1/2 was found in structures in which type I IL-1 receptor has already been identified as well as in structures lacking this receptor, activation of ERK1/2 is likely to occur in response to both direct and indirect action of interleukin-1beta on its target cells [35].
  • 2. Co-administration of IL-1 receptor antagonist (0.1 micrograms) with IL-1 beta (1 mu), IL-2 (10 mu) or IL-8 (0.1 mu) prevented the subsequent development of the hyperalgesia [36].

Analytical, diagnostic and therapeutic context of Il1r1


  1. Chronic hypoxia modulates the interleukin-1beta-stimulated inducible nitric oxide synthase pathway in cardiac myocytes. Kacimi, R., Long, C.S., Karliner, J.S. Circulation (1997) [Pubmed]
  2. Brain tumor development in rats is associated with changes in central nervous system cytokine and neuropeptide systems. Ilyin, S.E., Gayle, D., González-Gómez, I., Miele, M.E., Plata-Salamán, C.R. Brain Res. Bull. (1999) [Pubmed]
  3. IL-1 up-regulates osteopontin expression in experimental crescentic glomerulonephritis in the rat. Yu, X.Q., Fan, J.M., Nikolic-Paterson, D.J., Yang, N., Mu, W., Pichler, R., Johnson, R.J., Atkins, R.C., Lan, H.Y. Am. J. Pathol. (1999) [Pubmed]
  4. Central cyclooxygenase inhibitors reduced IL-1beta-induced hyperalgesia in temporomandibular joint of freely moving rats. Ahn, D.K., Chae, J.M., Choi, H.S., Kyung, H.M., Kwon, O.W., Park, H.S., Youn, D.H., Bae, Y.C. Pain (2005) [Pubmed]
  5. 3,4-Methylenedioxymethamphetamine increases interleukin-1beta levels and activates microglia in rat brain: studies on the relationship with acute hyperthermia and 5-HT depletion. Orio, L., O'Shea, E., Sanchez, V., Pradillo, J.M., Escobedo, I., Camarero, J., Moro, M.A., Green, A.R., Colado, M.I. J. Neurochem. (2004) [Pubmed]
  6. Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase. Corbett, J.A., McDaniel, M.L. J. Exp. Med. (1995) [Pubmed]
  7. The morphogenic/cytotoxic and prostaglandin-stimulating activities of interleukin-1 beta in the rat ovary are nitric oxide independent. Ben-Shlomo, I., Adashi, E.Y., Payne, D.W. J. Clin. Invest. (1994) [Pubmed]
  8. Induction of plasminogen activator inhibitor type 1 and type 1 collagen expression in rat cardiac microvascular endothelial cells by interleukin-1 and its dependence on oxygen-centered free radicals. Okada, H., Woodcock-Mitchell, J., Mitchell, J., Sakamoto, T., Marutsuka, K., Sobel, B.E., Fujii, S. Circulation (1998) [Pubmed]
  9. Interleukin-1 mediates a rapid inflammatory response after injection of adenoviral vectors into the brain. Cartmell, T., Southgate, T., Rees, G.S., Castro, M.G., Lowenstein, P.R., Luheshi, G.N. J. Neurosci. (1999) [Pubmed]
  10. Activation of vagal afferents after intravenous injection of interleukin-1beta: role of endogenous prostaglandins. Ek, M., Kurosawa, M., Lundeberg, T., Ericsson, A. J. Neurosci. (1998) [Pubmed]
  11. Evaluation of an interleukin-1 receptor antagonist in the rat acetic acid-induced colitis model. Thomas, T.K., Will, P.C., Srivastava, A., Wilson, C.L., Harbison, M., Little, J., Chesonis, R.S., Pignatello, M., Schmolze, D., Symington, J. Agents Actions (1991) [Pubmed]
  12. Granulocyte infiltration in experimental colitis in the rat is interleukin-1 dependent and leukotriene independent. McCafferty, D.M., Rioux, K.J., Wallace, J.L. Eicosanoids (1992) [Pubmed]
  13. Up-regulation of IL-1 receptor through PI3K/Akt is essential for the induction of iNOS gene expression in hepatocytes. Teshima, S., Nakanishi, H., Nishizawa, M., Kitagawa, K., Kaibori, M., Yamada, M., Habara, K., Kwon, A.H., Kamiyama, Y., Ito, S., Okumura, T. J. Hepatol. (2004) [Pubmed]
  14. Interleukin-1-induced neurotoxicity is mediated by glia and requires caspase activation and free radical release. Thornton, P., Pinteaux, E., Gibson, R.M., Allan, S.M., Rothwell, N.J. J. Neurochem. (2006) [Pubmed]
  15. Strain-dependent difference in inducible nitric oxide synthesis (iNOS) expression in rat pancreatic islets correlates with interferon regulating factor 1 (IRF-1) and heat shock protein 70 (HSP70) expression. Johannesen, J., Pociot, F., Karlsen, A.E., Mandrup-Poulsen, T., Nerup, J. Eur. Cytokine Netw. (2001) [Pubmed]
  16. Adenoviral overexpression of interleukin-1 receptor antagonist protein increases beta-cell replication in rat pancreatic islets. Téllez, N., Montolio, M., Biarnés, M., Castaño, E., Soler, J., Montanya, E. Gene Ther. (2005) [Pubmed]
  17. Induction of nitric oxide synthase activity by cytokines in ventricular myocytes is necessary but not sufficient to decrease contractile responsiveness to beta-adrenergic agonists. Ungureanu-Longrois, D., Balligand, J.L., Simmons, W.W., Okada, I., Kobzik, L., Lowenstein, C.J., Kunkel, S.L., Michel, T., Kelly, R.A., Smith, T.W. Circ. Res. (1995) [Pubmed]
  18. Interleukin-1beta enhances GABAA receptor cell-surface expression by a phosphatidylinositol 3-kinase/Akt pathway: relevance to sepsis-associated encephalopathy. Serantes, R., Arnalich, F., Figueroa, M., Salinas, M., Andrés-Mateos, E., Codoceo, R., Renart, J., Matute, C., Cavada, C., Cuadrado, A., Montiel, C. J. Biol. Chem. (2006) [Pubmed]
  19. Amphotericin B potentiates the activation of inducible nitric oxide synthase and causes nitric oxide-dependent mitochondrial dysfunction in cytokine-treated rodent astrocytes. Trajkovic, V., Markovic, M., Samardzic, T., Miljkovic, D.J., Popadic, D., Mostarica Stojkovic, M. Glia (2001) [Pubmed]
  20. Visualization and characterization of interleukin 1 receptors in brain. Farrar, W.L., Kilian, P.L., Ruff, M.R., Hill, J.M., Pert, C.B. J. Immunol. (1987) [Pubmed]
  21. In vivo transfer of engineered macrophages into the glomerulus: endogenous TGF-beta-mediated defense against macrophage-induced glomerular cell activation. Sütö, T.S., Fine, L.G., Shimizu, F., Kitamura, M. J. Immunol. (1997) [Pubmed]
  22. Pirfenidone inhibits the induction of iNOS stimulated by interleukin-1beta at a step of NF-kappaB DNA binding in hepatocytes. Nakanishi, H., Kaibori, M., Teshima, S., Yoshida, H., Kwon, A.H., Kamiyama, Y., Nishizawa, M., Ito, S., Okumura, T. J. Hepatol. (2004) [Pubmed]
  23. Induction of guanosine triphosphate-cyclohydrolase by follicle-stimulating hormone enhances interleukin-1 beta-stimulated nitric oxide synthase activity in granulosa cells. Tabraue, C., Diaz Peñate, R., Gallardo, G., Hernandez, I., Quintana, J., Lopez Blanco, F., Gonzalez Reyes, J., Fanjul, L.F., Ruiz de Galarreta, C.M. Endocrinology (1997) [Pubmed]
  24. Involvement of TLR4/type I IL-1 receptor signaling in the induction of inflammatory mediators and cell death induced by ethanol in cultured astrocytes. Blanco, A.M., Vallés, S.L., Pascual, M., Guerri, C. J. Immunol. (2005) [Pubmed]
  25. Modulation of rat mast cell reactivity by IL-1 beta. Divergent effects on nitric oxide and platelet-activating factor release. Hogaboam, C.M., Befus, A.D., Wallace, J.L. J. Immunol. (1993) [Pubmed]
  26. Interleukin-1 beta stimulates ovarian phosphoipase A2 (PLA2) expression and activity: up-regulation of both secretory and cytosolic PLA2. Kol, S., Ben-Shlomo, I., Ando, M., Payne, D.W., Adashi, E.Y. Endocrinology (1997) [Pubmed]
  27. IL-1 beta, IL-1 receptor type I and iNOS gene expression in rat brain vasculature and perivascular areas. Wong, M.L., Bongiorno, P.B., al-Shekhlee, A., Esposito, A., Khatri, P., Licinio, J. Neuroreport (1996) [Pubmed]
  28. Dibutyryl cyclic AMP and inflammatory cytokines mediate C3 expression in Schwann cells. Dashiell, S.M., Vanguri, P., Koski, C.L. Glia (1997) [Pubmed]
  29. The inhibitor cytokine interleukin-1 receptor antagonist synergistically augments cyclosporine immunosuppression in a rat cardiac allograft model. Shiraishi, M., Csete, M., Yasunaga, C., McDiarmid, S.V., Vannice, J.L., Busuttil, R.W., Shaked, A. J. Surg. Res. (1995) [Pubmed]
  30. Rat homolog of mouse interleukin-1 receptor accessory protein: cloning, localization and modulation studies. Liu, C., Chalmers, D., Maki, R., De Souza, E.B. J. Neuroimmunol. (1996) [Pubmed]
  31. Insulin-like growth factor I affects the intraovarian interleukin-1 system: evidence for suppression of type I interleukin-1 receptor expression and enhancement of secretory phospholipase A2 expression and activity. Kol, S., Ben-Shlomo, I., Ando, M., Adashi, E.Y. Mol. Hum. Reprod. (1997) [Pubmed]
  32. A novel nonhepatic hydroxycholesterol 7 alpha-hydroxylase that is markedly stimulated by interleukin-1 beta. Characterization in the immature rat ovary. Payne, D.W., Shackleton, C., Toms, H., Ben-Shlomo, I., Kol, S., deMoura, M., Strauss, J.F., Adashi, E.Y. J. Biol. Chem. (1995) [Pubmed]
  33. Learning modulation by endogenous hippocampal IL-1: blockade of endogenous IL-1 facilitates memory formation. Depino, A.M., Alonso, M., Ferrari, C., del Rey, A., Anthony, D., Besedovsky, H., Medina, J.H., Pitossi, F. Hippocampus. (2004) [Pubmed]
  34. Intracerebroventricular interleukin-1 alpha increases immunocyte beta-endorphin concentrations in the rat: involvement of corticotropin-releasing hormone, catecholamines, and serotonin. Sacerdote, P., Bianchi, M., Manfredi, B., Panerai, A.E. Endocrinology (1994) [Pubmed]
  35. Signaling pathways of interleukin-1 actions in the brain: anatomical distribution of phospho-ERK1/2 in the brain of rat treated systemically with interleukin-1beta. Nadjar, A., Combe, C., Busquet, P., Dantzer, R., Parnet, P. Neuroscience (2005) [Pubmed]
  36. The involvement of bradykinin B1 and B2 receptor mechanisms in cytokine-induced mechanical hyperalgesia in the rat. Davis, A.J., Perkins, M.N. Br. J. Pharmacol. (1994) [Pubmed]
  37. Concordant and discordant interleukin-1-mediated signaling in lung fibroblast thy-1 subpopulations. Hagood, J.S., Mangalwadi, A., Guo, B., MacEwen, M.W., Salazar, L., Fuller, G.M. Am. J. Respir. Cell Mol. Biol. (2002) [Pubmed]
  38. Interleukin-4 ameliorates experimental glomerulonephritis and up-regulates glomerular gene expression of IL-1 decoy receptor. Tam, F.W., Smith, J., Karkar, A.M., Pusey, C.D., Rees, A.J. Kidney Int. (1997) [Pubmed]
  39. Interleukin-1 beta (IL-1 beta) modulates prostaglandin production and the natural IL-1 receptor antagonist inhibits ovulation in the optimally stimulated rat ovarian perfusion model. Peterson, C.M., Hales, H.A., Hatasaka, H.H., Mitchell, M.D., Rittenhouse, L., Jones, K.P. Endocrinology (1993) [Pubmed]
  40. Expression of interleukin-1 beta in rat dorsal root ganglia. Copray, J.C., Mantingh, I., Brouwer, N., Biber, K., Küst, B.M., Liem, R.S., Huitinga, I., Tilders, F.J., Van Dam, A.M., Boddeke, H.W. J. Neuroimmunol. (2001) [Pubmed]
  41. The MAP kinase cascades are activated during post-ischemic liver reperfusion. Bendinelli, P., Piccoletti, R., Maroni, P., Bernelli-Zazzera, A. FEBS Lett. (1996) [Pubmed]
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