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1
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0028845730
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Cloning of a new cytokine that induces IFN-γ production by T cells
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Okamura H., Tsutsi H., Komatsu T., Yutsudo M., Hakura A., Tanimoto T., Torigoe K., Okura T., Nukada Y., Hattori K.et al. Cloning of a new cytokine that induces IFN-γ production by T cells. Nature. 378:1995;88-91.
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Nature
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Okamura, H.1
Tsutsi, H.2
Komatsu, T.3
Yutsudo, M.4
Hakura, A.5
Tanimoto, T.6
Torigoe, K.7
Okura, T.8
Nukada, Y.9
Hattori, K.10
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2
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0033491194
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Interleukin-18: A novel cytokine that augments both innate and acquired immunity
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Okamura H., Tsutsui H., Kashiwamura S., Yoshimoto T., Nakanishi K. Interleukin-18: a novel cytokine that augments both innate and acquired immunity. Adv Immunol. 70:1998;281-312.
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(1998)
Adv Immunol
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Okamura, H.1
Tsutsui, H.2
Kashiwamura, S.3
Yoshimoto, T.4
Nakanishi, K.5
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3
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0031749136
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Overview of interleukin-18: More than an interferon-γ inducing factor
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Dinarello C.A., Novick D., Puren A.J., Fantuzzi G., Shapiro L., Muhl H., Yoon D.Y., Reznikov L.L., Kim S.H., Rubinstein M. Overview of interleukin-18: more than an interferon-γ inducing factor. J Leukoc Biol. 63:1998;658-664.
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(1998)
J Leukoc Biol
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Dinarello, C.A.1
Novick, D.2
Puren, A.J.3
Fantuzzi, G.4
Shapiro, L.5
Muhl, H.6
Yoon, D.Y.7
Reznikov, L.L.8
Kim, S.H.9
Rubinstein, M.10
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5
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0031004174
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Caspase-1 processes IFN-γ-inducing factor and regulates LPS-induced IFN-γ production
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Ghayur T., Banerjee S., Hugunin M., Butler D., Herzog L., Carter A., Quintal L., Sekut L., Talanian R., Paskind M.et al. Caspase-1 processes IFN-γ-inducing factor and regulates LPS-induced IFN-γ production. Nature. 386:1997;619-623.
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Nature
, vol.386
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Ghayur, T.1
Banerjee, S.2
Hugunin, M.3
Butler, D.4
Herzog, L.5
Carter, A.6
Quintal, L.7
Sekut, L.8
Talanian, R.9
Paskind, M.10
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6
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15644369352
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Activation of interferon-γ inducing factor mediated by interleukin-1β converting enzyme
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Gu Y., Kuida K., Tsutsui H., Ku G., Hsiao K., Fleming M.A., Hayashi N., Higashino K., Okamura H., Nakanishi K.et al. Activation of interferon-γ inducing factor mediated by interleukin-1β converting enzyme. Science. 275:1997;206-209.
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(1997)
Science
, vol.275
, pp. 206-209
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Gu, Y.1
Kuida, K.2
Tsutsui, H.3
Ku, G.4
Hsiao, K.5
Fleming, M.A.6
Hayashi, N.7
Higashino, K.8
Okamura, H.9
Nakanishi, K.10
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7
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0031973493
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Lipopolysaccharide activates caspase-1(interleukin-1-converting enzyme) in cultured monocytic and endothelial cells
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Schumann R.R., Belka C., Reuter D., Lamping N., Kirschning C.J., Weber J.R., Pfeil D. Lipopolysaccharide activates caspase-1(interleukin-1-converting enzyme) in cultured monocytic and endothelial cells. Blood. 91:1998;577-584.
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(1998)
Blood
, vol.91
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Schumann, R.R.1
Belka, C.2
Reuter, D.3
Lamping, N.4
Kirschning, C.J.5
Weber, J.R.6
Pfeil, D.7
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8
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0031572443
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IL-18 accounts for both TNF-alpha- And Fas ligand-mediated hepatotoxic pathways in endotoxin-induced liver injury in mice
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Tsutsui H., Matsui K., Kawada N., Hyodo Y., Hayashi N., Okamura H., Higashino K., Nakanishi K. IL-18 accounts for both TNF-alpha- and Fas ligand-mediated hepatotoxic pathways in endotoxin-induced liver injury in mice. J Immunol. 159:1997;3961-3967.
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(1997)
J Immunol
, vol.159
, pp. 3961-3967
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Tsutsui, H.1
Matsui, K.2
Kawada, N.3
Hyodo, Y.4
Hayashi, N.5
Okamura, H.6
Higashino, K.7
Nakanishi, K.8
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9
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0030293444
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IFN-γ-inducing factor up-regulates Fas ligand-mediated cytotoxic activity of murine natural killer cell clones
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Tsutsui H., Nakanishi K., Matsui K., Higashino K., Okamura H., Miyazawa Y., Kaneda K. IFN-γ-inducing factor up-regulates Fas ligand-mediated cytotoxic activity of murine natural killer cell clones. J Immunol. 157:1996;3967-3973.
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(1996)
J Immunol
, vol.157
, pp. 3967-3973
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Tsutsui, H.1
Nakanishi, K.2
Matsui, K.3
Higashino, K.4
Okamura, H.5
Miyazawa, Y.6
Kaneda, K.7
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10
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0032990966
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IL-18-deficient mice are resistant to endotoxin-induced liver injury but highly susceptible to endotoxin shock
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The authors examined the role of IL-18 in liver injury and endotoxin shock in mice pretreated by Propionibacterium acnes and followed by low dose LPS administration. IL-18-deficient mice are resistant to liver injury; however, they are highly susceptible to endotoxin shock due to a high production of TNF-α. This indicates that IL-18 plays a role in protecting against endotoxin shock by downregulating TNF-α production
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Sakao Y., Takeda K., Tsutsui H., Kaisho T., Nomura F., Okamura H., Nakanishi K., Akira S. IL-18-deficient mice are resistant to endotoxin-induced liver injury but highly susceptible to endotoxin shock. Int Immunol. 11:1999;471-480. The authors examined the role of IL-18 in liver injury and endotoxin shock in mice pretreated by Propionibacterium acnes and followed by low dose LPS administration. IL-18-deficient mice are resistant to liver injury; however, they are highly susceptible to endotoxin shock due to a high production of TNF-α. This indicates that IL-18 plays a role in protecting against endotoxin shock by downregulating TNF-α production.
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(1999)
Int Immunol
, vol.11
, pp. 471-480
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Sakao, Y.1
Takeda, K.2
Tsutsui, H.3
Kaisho, T.4
Nomura, F.5
Okamura, H.6
Nakanishi, K.7
Akira, S.8
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11
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17544389276
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Interleukin-18 (interferon-γ-inducing factor) is produced by osteoblasts and acts via granulocyte/macrophage colony-stimulating factor and not via interferon-γ To inhibit osteoclast formation
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Udagawa N., Horwood N.J., Elliott J., Mackay A., Owens J., Okamura H., Kurimoto M., Chambers T.J., Martin T.J., Gillespie M.T. Interleukin-18 (interferon-γ-inducing factor) is produced by osteoblasts and acts via granulocyte/macrophage colony-stimulating factor and not via interferon-γ to inhibit osteoclast formation. J Exp Med. 185:1997;1005-1012.
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(1997)
J Exp Med
, vol.185
, pp. 1005-1012
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Udagawa, N.1
Horwood, N.J.2
Elliott, J.3
Mackay, A.4
Owens, J.5
Okamura, H.6
Kurimoto, M.7
Chambers, T.J.8
Martin, T.J.9
Gillespie, M.T.10
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12
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0032005857
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Interleukin 18 inhibits osteoclast formation via T cell production of granulocyte macrophage colony-stimulating factor
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Horwood N.J., Udagawa N., Elliott J., Grail D., Okamura H., Kurimoto M., Dunn A.R., Martin T., Gillespie M.T. Interleukin 18 inhibits osteoclast formation via T cell production of granulocyte macrophage colony-stimulating factor. J Clin Invest. 101:1998;595-603.
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(1998)
J Clin Invest
, vol.101
, pp. 595-603
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Horwood, N.J.1
Udagawa, N.2
Elliott, J.3
Grail, D.4
Okamura, H.5
Kurimoto, M.6
Dunn, A.R.7
Martin, T.8
Gillespie, M.T.9
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13
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0030851728
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Purification and characterization of the human interleukin-18 receptor
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Torigoe K., Ushio S., Okura T., Kobayashi S., Taniai M., Kunikata T., Murakami T., Sanou O., Kojima H., Fujii M.et al. Purification and characterization of the human interleukin-18 receptor. J Biol Chem. 272:1997;25737-25742.
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(1997)
J Biol Chem
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Torigoe, K.1
Ushio, S.2
Okura, T.3
Kobayashi, S.4
Taniai, M.5
Kunikata, T.6
Murakami, T.7
Sanou, O.8
Kojima, H.9
Fujii, M.10
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14
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0029989325
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IL-1Rrp is a novel receptor-like molecule similar to the type I interleukin-1 receptor and its homologues T1/ST2 and IL-1RAcP
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Parnet P., Garka K.E., Bonnert T.P., Dower S.K., Sims J.E. IL-1Rrp is a novel receptor-like molecule similar to the type I interleukin-1 receptor and its homologues T1/ST2 and IL-1RAcP. J Biol Chem. 271:1996;3967-3970.
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(1996)
J Biol Chem
, vol.271
, pp. 3967-3970
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Parnet, P.1
Garka, K.E.2
Bonnert, T.P.3
Dower, S.K.4
Sims, J.E.5
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15
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0032491599
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Cloning of a novel receptor subunit, AcPL, required for interleukin-18 signaling
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The authors have identified a novel member of the IL-1 receptor family, AcPL. In transient transfection assays, coexpression of IL-1Rrp and AcPL activated NF-κB and JNK in response to IL-18, although AcPL alone did not. A dominant-negative version of AcPL specifically inhibited IL-18 signaling. This finding indicates that AcPL is required for IL-18 signaling, analogous to the requirement for IL-1RAcP in IL-1 signaling
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Born T.L., Thomassen E., Bird T.A., Sims J.E. Cloning of a novel receptor subunit, AcPL, required for interleukin-18 signaling. J Biol Chem. 273:1998;29445-29450. The authors have identified a novel member of the IL-1 receptor family, AcPL. In transient transfection assays, coexpression of IL-1Rrp and AcPL activated NF-κB and JNK in response to IL-18, although AcPL alone did not. A dominant-negative version of AcPL specifically inhibited IL-18 signaling. This finding indicates that AcPL is required for IL-18 signaling, analogous to the requirement for IL-1RAcP in IL-1 signaling.
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(1998)
J Biol Chem
, vol.273
, pp. 29445-29450
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Born, T.L.1
Thomassen, E.2
Bird, T.A.3
Sims, J.E.4
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16
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0033136775
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Cutting edge: Generation of IL-18 receptor-deficient mice: Evidence for IL-1 receptor-related protein as an essential IL-18 binding receptor
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This paper describes the generation and characterization of IL-1RrP knockout mice. The data show that the IL-1Rrp is a ligand binding receptor that is essential for IL-18-mediated signaling events
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Hoshino K., Tsutsui H., Kawai T., Takeda K., Nakanishi K., Takeda Y., Akira S. Cutting edge: generation of IL-18 receptor-deficient mice: evidence for IL-1 receptor-related protein as an essential IL-18 binding receptor. J Immunol. 162:1999;5041-5044. This paper describes the generation and characterization of IL-1RrP knockout mice. The data show that the IL-1Rrp is a ligand binding receptor that is essential for IL-18-mediated signaling events.
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(1999)
J Immunol
, vol.162
, pp. 5041-5044
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Hoshino, K.1
Tsutsui, H.2
Kawai, T.3
Takeda, K.4
Nakanishi, K.5
Takeda, Y.6
Akira, S.7
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17
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0032983336
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Interleukin-18 binding protein: A novel modulator of the Th1 cytokine response
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This is the first report of the molecular cloning and characterization of a novel IL-18 binding protein. IL-18 binding protein is a member of the immunoglobulin superfamily but lacks the transmembrane domain and consists of only the extracellular domain of the ligand binding receptor. IL-18 binding protein prevents IL-18-mediated function, similar to neutralizing antibodies to IL-18
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Novick D., Kim S.H., Fantuzzi G., Reznikov L.L., Dinarello C.A., Rubinstein M. Interleukin-18 binding protein: a novel modulator of the Th1 cytokine response. Immunity. 10:1999;127-136. This is the first report of the molecular cloning and characterization of a novel IL-18 binding protein. IL-18 binding protein is a member of the immunoglobulin superfamily but lacks the transmembrane domain and consists of only the extracellular domain of the ligand binding receptor. IL-18 binding protein prevents IL-18-mediated function, similar to neutralizing antibodies to IL-18.
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(1999)
Immunity
, vol.10
, pp. 127-136
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Novick, D.1
Kim, S.H.2
Fantuzzi, G.3
Reznikov, L.L.4
Dinarello, C.A.5
Rubinstein, M.6
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18
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0032424107
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MyD genes in negative growth control
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Lieberman D.A., Hoffman B. MyD genes in negative growth control. Oncogene. 17:1998;3319-3329.
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(1998)
Oncogene
, vol.17
, pp. 3319-3329
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Lieberman, D.A.1
Hoffman, B.2
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19
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0030694235
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IGIF does not drive Th1 development but synergizes with IL-12 for interferon-γ production and activates IRAK and NF-κB
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Robinson D., Shibuya K., Mui A., Zonin F., Murphy E., Sana T., Hartley S.B., Monon S., Kastelein R., Bazan F.et al. IGIF does not drive Th1 development but synergizes with IL-12 for interferon-γ production and activates IRAK and NF-κB. Immunity. 7:1997;571-581.
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(1997)
Immunity
, vol.7
, pp. 571-581
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Robinson, D.1
Shibuya, K.2
Mui, A.3
Zonin, F.4
Murphy, E.5
Sana, T.6
Hartley, S.B.7
Monon, S.8
Kastelein, R.9
Bazan, F.10
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20
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0032489224
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Interleukin-18 activates the IRAK-TRAF6 pathway in mouse EL-4 cells
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Kojima H., Takeuchi M., Ohta T., Nishida Y., Arai N., Ikeda M., Ikegami H., Kurimoto M. Interleukin-18 activates the IRAK-TRAF6 pathway in mouse EL-4 cells. Biochem Biophys Res Commun. 244:1998;183-186.
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(1998)
Biochem Biophys Res Commun
, vol.244
, pp. 183-186
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Kojima, H.1
Takeuchi, M.2
Ohta, T.3
Nishida, Y.4
Arai, N.5
Ikeda, M.6
Ikegami, H.7
Kurimoto, M.8
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21
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0031578229
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Interleukin-18 activates NF-κB in murine T helper type 1 cells
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Matsumoto S., Tuji-Takayama K., Aizawa Y., Koide K., Takeuchi M., Ohta T., Kurimoto M. Interleukin-18 activates NF-κB in murine T helper type 1 cells. Biochem Biophys Res Commun. 234:1997;454-457.
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(1997)
Biochem Biophys Res Commun
, vol.234
, pp. 454-457
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Matsumoto, S.1
Tuji-Takayama, K.2
Aizawa, Y.3
Koide, K.4
Takeuchi, M.5
Ohta, T.6
Kurimoto, M.7
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22
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0032127279
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Targeted disruption of the MyD88 gene results in loss of IL-1- And IL-18-mediated function
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The authors generated mice lacking MyD88, the adaptor molecule involved in IL-1 signaling. The mutant mice had defects in IL-1-mediated functions such as T cell proliferation, induction of acute phase proteins and inflammatory cytokines. MyD88-deficient mice also had defects in IL-18-mediated functions including NK cell activity, IFN-γ production from Th1 cells, and in vivo Th1 response. These results demonstrate that MyD88 is a critical component in the signaling cascade that is mediated by IL-1 receptor as well as IL-18 receptor
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Adachi O., Kawai T., Takeda K., Matsumoto M., Tsutsui H., Sakagami M., Nakanishi K., Akira S. Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function. Immunity. 9:1998;143-150. The authors generated mice lacking MyD88, the adaptor molecule involved in IL-1 signaling. The mutant mice had defects in IL-1-mediated functions such as T cell proliferation, induction of acute phase proteins and inflammatory cytokines. MyD88-deficient mice also had defects in IL-18-mediated functions including NK cell activity, IFN-γ production from Th1 cells, and in vivo Th1 response. These results demonstrate that MyD88 is a critical component in the signaling cascade that is mediated by IL-1 receptor as well as IL-18 receptor.
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(1998)
Immunity
, vol.9
, pp. 143-150
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Adachi, O.1
Kawai, T.2
Takeda, K.3
Matsumoto, M.4
Tsutsui, H.5
Sakagami, M.6
Nakanishi, K.7
Akira, S.8
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23
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0033526110
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Defective interleukin (IL)-18-mediated natural killer and T helper cell type 1 responses in IL-1 receptor-associated kinase (IRAK)-deficient mice
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This paper reveals the role of IRAK in IL-18-mediated responses by gene targeting. Significant defects in JNK activation and partial impairment in NF-κB activation were found in IRAK-deficient Th1 cells. IFN-γ production and induction of NK cell cytotoxicity in response to IL-18 were severely impaired, demonstrating that IRAK plays an important role in IL-18-mediated signaling and function
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Kanakaraj P., Ngo K., Wu Y., Angulo A., Ghazal P., Harris C.A., Siekierka J.J., Peterson P.A., Fung-Leung W.P. Defective interleukin (IL)-18-mediated natural killer and T helper cell type 1 responses in IL-1 receptor-associated kinase (IRAK)-deficient mice. J Exp Med. 189:1999;1129-1138. This paper reveals the role of IRAK in IL-18-mediated responses by gene targeting. Significant defects in JNK activation and partial impairment in NF-κB activation were found in IRAK-deficient Th1 cells. IFN-γ production and induction of NK cell cytotoxicity in response to IL-18 were severely impaired, demonstrating that IRAK plays an important role in IL-18-mediated signaling and function.
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(1999)
J Exp Med
, vol.189
, pp. 1129-1138
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Kanakaraj, P.1
Ngo, K.2
Wu, Y.3
Angulo, A.4
Ghazal, P.5
Harris, C.A.6
Siekierka, J.J.7
Peterson, P.A.8
Fung-Leung, W.P.9
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24
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0031230444
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A mechanism underlying synergy between IL-12 and IFN-γ-inducing factor in enhanced production of IFN-γ
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Ahn H.J., Maruo S., Tomura M., Mu J., Hamaoka T., Nakanishi K., Clark S., Kurimoto M., Okamura H., Fujiwara H. A mechanism underlying synergy between IL-12 and IFN-γ-inducing factor in enhanced production of IFN-γ J Immunol. 159:1997;2125-2131.
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(1997)
J Immunol
, vol.159
, pp. 2125-2131
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Ahn, H.J.1
Maruo, S.2
Tomura, M.3
Mu, J.4
Hamaoka, T.5
Nakanishi, K.6
Clark, S.7
Kurimoto, M.8
Okamura, H.9
Fujiwara, H.10
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25
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0032193770
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IL-12 up-regulates IL-18 receptor expression on T cells, Th1 cells, B cells: Synergism with IL-18 for IFN-γ production
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The authors demonstrate that IL-12 and IL-18 promptly and synergistically induce T and B cells to develop into IFN-γ-producing cells without engaging their antigen receptors. Although they do not become memory cells, this early and drastic induction of IFN-γ may play a role in innate immunity
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Yoshimoto T., Takeda K., Tanaka T., Ohkusu K., Kashiwamura S., Okamura H., Akira S., Nakanishi K. IL-12 up-regulates IL-18 receptor expression on T cells, Th1 cells, B cells: synergism with IL-18 for IFN-γ production. J Immunol. 161:1998;3400-3407. The authors demonstrate that IL-12 and IL-18 promptly and synergistically induce T and B cells to develop into IFN-γ-producing cells without engaging their antigen receptors. Although they do not become memory cells, this early and drastic induction of IFN-γ may play a role in innate immunity.
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(1998)
J Immunol
, vol.161
, pp. 3400-3407
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Yoshimoto, T.1
Takeda, K.2
Tanaka, T.3
Ohkusu, K.4
Kashiwamura, S.5
Okamura, H.6
Akira, S.7
Nakanishi, K.8
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26
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3643120790
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Selective expression and functions of interleukin 18 receptor on T helper (Th) type 1 but not Th2 cells
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This paper shows that IL-18R is selectively expressed on murine Th1 but not Th2 cells, and the synergistic effect of IL-12 and IL-18 on Th1 development may be due to the reciprocal upregulation of their receptors
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Xu D., Chan W.L., Leung B.P., Hunter D., Schulz K., Carter R.W., McInnes I.B., Robinson J.H., Liew F.Y. Selective expression and functions of interleukin 18 receptor on T helper (Th) type 1 but not Th2 cells. J Exp Med. 188:1998;1485-1492. This paper shows that IL-18R is selectively expressed on murine Th1 but not Th2 cells, and the synergistic effect of IL-12 and IL-18 on Th1 development may be due to the reciprocal upregulation of their receptors.
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(1998)
J Exp Med
, vol.188
, pp. 1485-1492
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Xu, D.1
Chan, W.L.2
Leung, B.P.3
Hunter, D.4
Schulz, K.5
Carter, R.W.6
McInnes, I.B.7
Robinson, J.H.8
Liew, F.Y.9
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27
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0032521933
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IL-12 and IL-18 differentially regulate the transcriptional activity of the human IFN-γ promoter in primary CD4+ T lymphocytes
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+ T cells. In transient transfection assays, they showed that both AP-1 and STAT4 are required for IL-12-dependent IFN-γ promoter activity, whereas IL-18 causes direct activation via AP-1
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+ T cells. In transient transfection assays, they showed that both AP-1 and STAT4 are required for IL-12-dependent IFN-γ promoter activity, whereas IL-18 causes direct activation via AP-1.
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(1998)
J Immunol
, vol.160
, pp. 3642-3647
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Barbulescu, K.1
Becker, C.2
Schlaak, J.F.3
Schmitt, E.4
Meyer Zum Buschenfelde, K.H.5
Neurath, M.F.6
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28
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0033583431
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Lineage-specific requirement for signal transducer and activator of transcription (Stat)4 in interferon γ production from CD4(+) versus CD8(+) T cells
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Carter L.L., Murphy K.M. Lineage-specific requirement for signal transducer and activator of transcription (Stat)4 in interferon γ production from CD4(+) versus CD8(+) T cells. J Exp Med. 189:1999;1355-1360.
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(1999)
J Exp Med
, vol.189
, pp. 1355-1360
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Carter, L.L.1
Murphy, K.M.2
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29
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0033136283
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An essential role for NF-κB in IL-18-induced IFN-γ expression in KG-1 cells
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Kojima H., Aizawa Y., Yanai Y., Nagaoka K., Takeuchi M., Ohta T., Ikegami H., Ikeda M., Kurimoto M. An essential role for NF-κB in IL-18-induced IFN-γ expression in KG-1 cells. J Immunol. 162:1999;5063-5069.
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(1999)
J Immunol
, vol.162
, pp. 5063-5069
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Kojima, H.1
Aizawa, Y.2
Yanai, Y.3
Nagaoka, K.4
Takeuchi, M.5
Ohta, T.6
Ikegami, H.7
Ikeda, M.8
Kurimoto, M.9
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30
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0033084021
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IL-18 up-regulates perforin-mediated NK activity without increasing perforin messenger RNA expression by binding to constitutively expressed IL-18 receptor
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This paper shows that IL-18 and IL-12 independently upregulate NK activity. Without endogenous IL-12, NK cells expressed IL-18R and IL-18 augmented NK cell activity
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Hyodo Y., Matsui K., Hayashi N., Tsutsui H., Kashiwamura S., Yamauchi H., Hiroishi K., Takeda K., Tagawa Y., Iwakura Y.et al. IL-18 up-regulates perforin-mediated NK activity without increasing perforin messenger RNA expression by binding to constitutively expressed IL-18 receptor. J Immunol. 162:1999;1662-1668. This paper shows that IL-18 and IL-12 independently upregulate NK activity. Without endogenous IL-12, NK cells expressed IL-18R and IL-18 augmented NK cell activity.
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(1999)
J Immunol
, vol.162
, pp. 1662-1668
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Hyodo, Y.1
Matsui, K.2
Hayashi, N.3
Tsutsui, H.4
Kashiwamura, S.5
Yamauchi, H.6
Hiroishi, K.7
Takeda, K.8
Tagawa, Y.9
Iwakura, Y.10
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31
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18844481515
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Defective NK cell activity and Th1 response in IL-18-deficient mice
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This paper documents the generation and characterization of IL-18 knockout mice. These mice display reduced production of IFN-γ, impaired NK cell activity and a defective in vivo Th1 cell response. These defects were not complete, however, as shown in IL-12 knockout mice. The authors therefore generated mice lacking both IL-18 and IL-12. In these double knockout mice, NK activity and in vivo Th1 response were further impaired, demonstrating the important role of both IL-18 and IL-12 in NK activity and Th1 response
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Takeda K., Tsutsui H., Yoshimoto T., Adachi O., Yoshida N., Kishimoto T., Okamura H., Nakanishi K., Akira S. Defective NK cell activity and Th1 response in IL-18-deficient mice. Immunity. 8:1998;383-390. This paper documents the generation and characterization of IL-18 knockout mice. These mice display reduced production of IFN-γ, impaired NK cell activity and a defective in vivo Th1 cell response. These defects were not complete, however, as shown in IL-12 knockout mice. The authors therefore generated mice lacking both IL-18 and IL-12. In these double knockout mice, NK activity and in vivo Th1 response were further impaired, demonstrating the important role of both IL-18 and IL-12 in NK activity and Th1 response.
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(1998)
Immunity
, vol.8
, pp. 383-390
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Takeda, K.1
Tsutsui, H.2
Yoshimoto, T.3
Adachi, O.4
Yoshida, N.5
Kishimoto, T.6
Okamura, H.7
Nakanishi, K.8
Akira, S.9
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32
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0032526840
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Murine macrophages secrete interferon γ upon combined stimulation with interleukin (IL)-12 and IL-18: A novel pathway of autocrine macrophage activation
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This paper demonstrates that macrophages are not only a key cell-type responding to IFN-γ but are also potent IFN-γ-producing cells
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Munder M., Mallo M., Eichmann K., Modolell M. Murine macrophages secrete interferon γ upon combined stimulation with interleukin (IL)-12 and IL-18: a novel pathway of autocrine macrophage activation. J Exp Med. 187:1998;2103-2108. This paper demonstrates that macrophages are not only a key cell-type responding to IFN-γ but are also potent IFN-γ-producing cells.
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(1998)
J Exp Med
, vol.187
, pp. 2103-2108
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Munder, M.1
Mallo, M.2
Eichmann, K.3
Modolell, M.4
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33
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0033136326
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IL-18 is a potent coinducer of IL-13 in NK and T cells: A new potential role for IL-18 in modulating the immune response
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This is the first report showing that IL-18 is a strong inducer of IL-13 from NK and T cells in the presence of IL-2. This presents the possibility that IL-18 may participate in Th2 response under the condition that IFN-γ production is downregulated
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Hoshino T., Wiltrout R.H., Young H.A. IL-18 is a potent coinducer of IL-13 in NK and T cells: a new potential role for IL-18 in modulating the immune response. J Immunol. 162:1999;5070-5077. This is the first report showing that IL-18 is a strong inducer of IL-13 from NK and T cells in the presence of IL-2. This presents the possibility that IL-18 may participate in Th2 response under the condition that IFN-γ production is downregulated.
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(1999)
J Immunol
, vol.162
, pp. 5070-5077
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Hoshino, T.1
Wiltrout, R.H.2
Young, H.A.3
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34
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0033152023
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IL-18, a novel immunoregulatory cytokine, is up-regulated in Crohn's disease: Expression and localization in intestinal mucosal cells
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Pizarro T.T., Michie M.H., Bentz M., Woraratanadharm J., Smith M.F. Jr., Foley E., Moskaluk C.A., Bickston S.J., Cominelli F. IL-18, a novel immunoregulatory cytokine, is up-regulated in Crohn's disease: expression and localization in intestinal mucosal cells. J Immunol. 162:1999;6829-6835.
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(1999)
J Immunol
, vol.162
, pp. 6829-6835
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Pizarro, T.T.1
Michie, M.H.2
Bentz, M.3
Woraratanadharm, J.4
Smith M.F., Jr.5
Foley, E.6
Moskaluk, C.A.7
Bickston, S.J.8
Cominelli, F.9
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35
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0032213360
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Prevention of Th2-like cell responses by coadministration of IL-12 and IL-18 is associated with inhibition of antigen-induced airway hyperresponsiveness, eosinophilia, and serum IgE levels
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Hofstra C.L., Van Ark I., Hofman G., Kool M., Nijkamp F.P., Van Oosterhout A.J. Prevention of Th2-like cell responses by coadministration of IL-12 and IL-18 is associated with inhibition of antigen-induced airway hyperresponsiveness, eosinophilia, and serum IgE levels. J Immunol. 161:1998;5054-5060.
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(1998)
J Immunol
, vol.161
, pp. 5054-5060
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Hofstra, C.L.1
Van Ark, I.2
Hofman, G.3
Kool, M.4
Nijkamp, F.P.5
Van Oosterhout, A.J.6
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