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Volumn 15, Issue 4, 2003, Pages 396-401

Recognition of microbial infection by Toll-like receptors

Author keywords

[No Author keywords available]

Indexed keywords

ADAPTOR PROTEIN; GENE PRODUCT; INTERFERON REGULATORY FACTOR 3; INTERLEUKIN 1 RECEPTOR ASSOCIATED PROTEIN; INTERLEUKIN 1 RECEPTOR DOMAIN CONTAINING ADAPTER INDUCING INTERFERON BETA; PROTEIN; TOLL LIKE RECEPTOR; TOLL LIKE RECEPTOR 2; TOLL LIKE RECEPTOR 3; TOLL LIKE RECEPTOR 4; TOLL LIKE RECEPTOR 5; TOLL LIKE RECEPTOR 7; TOLL LIKE RECEPTOR 8; TOLL LIKE RECEPTOR 9; TRANSCRIPTION FACTOR; UNCLASSIFIED DRUG;

EID: 0042405132     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(03)00080-3     Document Type: Review
Times cited : (483)

References (51)
  • 2
    • 0035524488 scopus 로고    scopus 로고
    • Toll-like receptors and innate immunity
    • Medzhitov R. Toll-like receptors and innate immunity. Nat Rev Immunol. 1:2001;135-145.
    • (2001) Nat Rev Immunol , vol.1 , pp. 135-145
    • Medzhitov, R.1
  • 4
    • 0037061453 scopus 로고    scopus 로고
    • Chromatin-IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors
    • This paper demonstrates that engagement of TLR9 on B cells by chromatin-containing immune complexes can lead to the activation of autoreactive B cells
    • Leadbetter E.A., Rifkin I.R., Hohlbaum A.M., Beaudette B.C., Shlomchik M.J., Marshak-Rothstein A. Chromatin-IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors. Nature. 416:2002;603-607 This paper demonstrates that engagement of TLR9 on B cells by chromatin-containing immune complexes can lead to the activation of autoreactive B cells.
    • (2002) Nature , vol.416 , pp. 603-607
    • Leadbetter, E.A.1    Rifkin, I.R.2    Hohlbaum, A.M.3    Beaudette, B.C.4    Shlomchik, M.J.5    Marshak-Rothstein, A.6
  • 5
    • 0036839577 scopus 로고    scopus 로고
    • Endogenous ligands of Toll-like receptors: Implications for regulating inflammatory and immune responses
    • Beg A.A. Endogenous ligands of Toll-like receptors: implications for regulating inflammatory and immune responses. Trends Immunol. 23:2002;509-512.
    • (2002) Trends Immunol , vol.23 , pp. 509-512
    • Beg, A.A.1
  • 7
    • 0037414787 scopus 로고    scopus 로고
    • Endotoxin contamination in recombinant human heat shock protein 70 (Hsp70) preparation is responsible for the induction of tumor necrosis factor alpha release by murine macrophages
    • Gao B., Tsan M.F. Endotoxin contamination in recombinant human heat shock protein 70 (Hsp70) preparation is responsible for the induction of tumor necrosis factor alpha release by murine macrophages. J Biol Chem. 278:2003;174-179.
    • (2003) J Biol Chem , vol.278 , pp. 174-179
    • Gao, B.1    Tsan, M.F.2
  • 8
    • 0035877013 scopus 로고    scopus 로고
    • An essential role of the NF-kappa B/Toll-like receptor pathway in induction of inflammatory and tissue-repair gene expression by necrotic cells
    • Li M., Carpio D.F., Zheng Y., Bruzzo P., Singh V., Ouaaz F., Medzhitov R.M., Beg A.A. An essential role of the NF-kappa B/Toll-like receptor pathway in induction of inflammatory and tissue-repair gene expression by necrotic cells. J Immunol. 166:2001;7128-7135.
    • (2001) J Immunol , vol.166 , pp. 7128-7135
    • Li, M.1    Carpio, D.F.2    Zheng, Y.3    Bruzzo, P.4    Singh, V.5    Ouaaz, F.6    Medzhitov, R.M.7    Beg, A.A.8
  • 9
    • 0034795208 scopus 로고    scopus 로고
    • Endoplasmic reticulum chaperone gp96 is required for innate immunity but not cell viability
    • Randow F., Seed B. Endoplasmic reticulum chaperone gp96 is required for innate immunity but not cell viability. Nat Cell Biol. 3:2001;891-896.
    • (2001) Nat Cell Biol , vol.3 , pp. 891-896
    • Randow, F.1    Seed, B.2
  • 10
    • 0034927975 scopus 로고    scopus 로고
    • Dendritic-cell function in Toll-like receptor- and MyD88-knockout mice
    • Kaisho T., Akira S. Dendritic-cell function in Toll-like receptor- and MyD88-knockout mice. Trends Immunol. 22:2001;78-83.
    • (2001) Trends Immunol , vol.22 , pp. 78-83
    • Kaisho, T.1    Akira, S.2
  • 11
    • 0037436119 scopus 로고    scopus 로고
    • Toll pathway-dependent blockade of CD4+CD25+ T cell-mediated suppression by dendritic cells
    • Pasare C., Medzhitov R. Toll pathway-dependent blockade of CD4+CD25+ T cell-mediated suppression by dendritic cells. Science. 299:2003;1033-1036.
    • (2003) Science , vol.299 , pp. 1033-1036
    • Pasare, C.1    Medzhitov, R.2
  • 12
    • 0029865142 scopus 로고    scopus 로고
    • IRAK: A kinase associated with the interleukin-1 receptor
    • Cao Z., Henzel W.J., Gao X. IRAK: a kinase associated with the interleukin-1 receptor. Science. 271:1996;1128-1131.
    • (1996) Science , vol.271 , pp. 1128-1131
    • Cao, Z.1    Henzel, W.J.2    Gao, X.3
  • 13
    • 0037117543 scopus 로고    scopus 로고
    • IRAK-4: A novel member of the IRAK family with the properties of an IRAK-kinase
    • Li S., Strelow A., Fontana E.J., Wesche H. IRAK-4: a novel member of the IRAK family with the properties of an IRAK-kinase. Proc Natl Acad Sci USA. 99:2002;5567-5572.
    • (2002) Proc Natl Acad Sci USA , vol.99 , pp. 5567-5572
    • Li, S.1    Strelow, A.2    Fontana, E.J.3    Wesche, H.4
  • 14
    • 0030694108 scopus 로고    scopus 로고
    • IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling
    • Muzio M., Ni J., Feng P., Dixit V.M. IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling. Science. 278:1997;1612-1615.
    • (1997) Science , vol.278 , pp. 1612-1615
    • Muzio, M.1    Ni, J.2    Feng, P.3    Dixit, V.M.4
  • 15
    • 0033516561 scopus 로고    scopus 로고
    • IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family
    • Wesche H., Gao X., Li X., Kirschning C.J., Stark G.R., Cao Z. IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family. J Biol Chem. 274:1999;19403-19410.
    • (1999) J Biol Chem , vol.274 , pp. 19403-19410
    • Wesche, H.1    Gao, X.2    Li, X.3    Kirschning, C.J.4    Stark, G.R.5    Cao, Z.6
  • 16
    • 0037178785 scopus 로고    scopus 로고
    • IRAK-M is a negative regulator of Toll-like receptor signaling
    • IRAK-M is a kinase-inactive IRAK family member expressed in monocytes and macrophages, and is induced upon TLR stimulation. Surprisingly, this IRAK inhibits cytokine production resulting from TLR signaling. IRAK-M-deficient mice have enhanced inflammatory responses to bacterial infection, indicating that IRAK-M dampens this response
    • Kobayashi K., Hernandez L.D., Galan J.E., Janeway C.A. Jr., Medzhitov R., Flavell R.A. IRAK-M is a negative regulator of Toll-like receptor signaling. Cell. 110:2002;191-202 IRAK-M is a kinase-inactive IRAK family member expressed in monocytes and macrophages, and is induced upon TLR stimulation. Surprisingly, this IRAK inhibits cytokine production resulting from TLR signaling. IRAK-M-deficient mice have enhanced inflammatory responses to bacterial infection, indicating that IRAK-M dampens this response.
    • (2002) Cell , vol.110 , pp. 191-202
    • Kobayashi, K.1    Hernandez, L.D.2    Galan, J.E.3    Janeway C.A., Jr.4    Medzhitov, R.5    Flavell, R.A.6
  • 17
    • 0037129212 scopus 로고    scopus 로고
    • Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4
    • In this paper, the authors generate and analyze IRAK-4 knockout mice, revealing an essential role for IRAK-4 in TLR signaling. These mice have striking impairments in the ability to produce cytokines (IL-1, TNF and IL-6) both in vitro and in vivo as a result of IL-1 or TLR stimulation. The animals are also resistant to lethal septic shock (a TLR4 response) and are dramatically more susceptible to bacterial and viral infections than wild-type animals
    • Suzuki N., Suzuki S., Duncan G.S., Millar D.G., Wada T., Mirtsos C., Takada H., Wakeham A., Itie A., Li S.et al. Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4. Nature. 416:2002;750-756 In this paper, the authors generate and analyze IRAK-4 knockout mice, revealing an essential role for IRAK-4 in TLR signaling. These mice have striking impairments in the ability to produce cytokines (IL-1, TNF and IL-6) both in vitro and in vivo as a result of IL-1 or TLR stimulation. The animals are also resistant to lethal septic shock (a TLR4 response) and are dramatically more susceptible to bacterial and viral infections than wild-type animals.
    • (2002) Nature , vol.416 , pp. 750-756
    • Suzuki, N.1    Suzuki, S.2    Duncan, G.S.3    Millar, D.G.4    Wada, T.5    Mirtsos, C.6    Takada, H.7    Wakeham, A.8    Itie, A.9    Li, S.10
  • 19
    • 0035339861 scopus 로고    scopus 로고
    • Endotoxin-induced maturation of MyD88-deficient dendritic cells
    • Kaisho T., Takeuchi O., Kawai T., Hoshino K., Akira S. Endotoxin-induced maturation of MyD88-deficient dendritic cells. J Immunol. 166:2001;5688-5694.
    • (2001) J Immunol , vol.166 , pp. 5688-5694
    • Kaisho, T.1    Takeuchi, O.2    Kawai, T.3    Hoshino, K.4    Akira, S.5
  • 20
    • 0033166472 scopus 로고    scopus 로고
    • Unresponsiveness of MyD88-deficient mice to endotoxin
    • Kawai T., Adachi O., Ogawa T., Takeda K., Akira S. Unresponsiveness of MyD88-deficient mice to endotoxin. Immunity. 11:1999;115-122.
    • (1999) Immunity , vol.11 , pp. 115-122
    • Kawai, T.1    Adachi, O.2    Ogawa, T.3    Takeda, K.4    Akira, S.5
  • 21
    • 0034650420 scopus 로고    scopus 로고
    • Cutting edge: Preferentially the R-stereoisomer of the mycoplasmal lipopeptide macrophage-activating lipopeptide-2 activates immune cells through a toll-like receptor 2- and MyD88-dependent signaling pathway
    • Takeuchi O., Kaufmann A., Grote K., Kawai T., Hoshino K., Morr M., Muhlradt P.F., Akira S. Cutting edge: preferentially the R-stereoisomer of the mycoplasmal lipopeptide macrophage-activating lipopeptide-2 activates immune cells through a toll-like receptor 2- and MyD88-dependent signaling pathway. J Immunol. 164:2000;554-557.
    • (2000) J Immunol , vol.164 , pp. 554-557
    • Takeuchi, O.1    Kaufmann, A.2    Grote, K.3    Kawai, T.4    Hoshino, K.5    Morr, M.6    Muhlradt, P.F.7    Akira, S.8
  • 22
    • 0034699340 scopus 로고    scopus 로고
    • Recognition of CpG DNA is mediated by signaling pathways dependent on the adaptor protein MyD88
    • Schnare M., Holt A.C., Takeda K., Akira S., Medzhitov R. Recognition of CpG DNA is mediated by signaling pathways dependent on the adaptor protein MyD88. Curr Biol. 10:2000;1139-1142.
    • (2000) Curr Biol , vol.10 , pp. 1139-1142
    • Schnare, M.1    Holt, A.C.2    Takeda, K.3    Akira, S.4    Medzhitov, R.5
  • 23
    • 0035889228 scopus 로고    scopus 로고
    • Lipopolysaccharide stimulates the MyD88-independent pathway and results in activation of IFN-regulatory factor 3 and the expression of a subset of lipopolysaccharide-inducible genes
    • Kawai T., Takeuchi O., Fujita T., Inoue J., Muhlradt P.F., Sato S., Hoshino K., Akira S. Lipopolysaccharide stimulates the MyD88-independent pathway and results in activation of IFN-regulatory factor 3 and the expression of a subset of lipopolysaccharide-inducible genes. J Immunol. 167:2001;5887-5894.
    • (2001) J Immunol , vol.167 , pp. 5887-5894
    • Kawai, T.1    Takeuchi, O.2    Fujita, T.3    Inoue, J.4    Muhlradt, P.F.5    Sato, S.6    Hoshino, K.7    Akira, S.8
  • 24
    • 0035555301 scopus 로고    scopus 로고
    • TIRAP: An adapter molecule in the Toll signaling pathway
    • Horng T., Barton G.M., Medzhitov R. TIRAP: an adapter molecule in the Toll signaling pathway. Nat Immunol. 2:2001;835-841.
    • (2001) Nat Immunol , vol.2 , pp. 835-841
    • Horng, T.1    Barton, G.M.2    Medzhitov, R.3
  • 27
    • 0037153130 scopus 로고    scopus 로고
    • The adaptor molecule TIRAP provides signalling specificity for Toll-like receptors
    • •] describe the phenotype of TIRAP deficient mice. These mice have impaired B-cell proliferation and cytokine production in response to stimulation with TLR2 and TLR4 ligands but not with other TLR ligands, indicating differences in the signal transduction pathways among TLRs
    • •] describe the phenotype of TIRAP deficient mice. These mice have impaired B-cell proliferation and cytokine production in response to stimulation with TLR2 and TLR4 ligands but not with other TLR ligands, indicating differences in the signal transduction pathways among TLRs.
    • (2002) Nature , vol.420 , pp. 329-333
    • Horng, T.1    Barton, G.M.2    Flavell, R.A.3    Medzhitov, R.4
  • 29
    • 0037114185 scopus 로고    scopus 로고
    • Cutting edge: A novel Toll/IL-1 receptor domain-containing adapter that preferentially activates the IFN-beta promoter in the Toll-like receptor signaling
    • •] describe a novel adaptor protein that links TLR activation with the induction of IRF3. Because IRF3 is involved in IFN-β production, TLRs utilizing this adapter could potentially stimulate an antiviral response. TRIF/TICAM appears to operate downstream of a only a subset of TLRS. Both papers demonstrate that TRIF/TICAM can interact directly with TLR3 and can activate the IFN-β promoter
    • •] describe a novel adaptor protein that links TLR activation with the induction of IRF3. Because IRF3 is involved in IFN-β production, TLRs utilizing this adapter could potentially stimulate an antiviral response. TRIF/TICAM appears to operate downstream of a only a subset of TLRS. Both papers demonstrate that TRIF/TICAM can interact directly with TLR3 and can activate the IFN-β promoter.
    • (2002) J Immunol , vol.169 , pp. 6668-6672
    • Yamamoto, M.1    Sato, S.2    Mori, K.3    Hoshino, K.4    Takeuchi, O.5    Takeda, K.6    Akira, S.7
  • 30
    • 0036785557 scopus 로고    scopus 로고
    • MyD88-dependent but Toll-like receptor 2-independent innate immunity to Listeria: No role for either in macrophage listericidal activity
    • Edelson B.T., Unanue E.R. MyD88-dependent but Toll-like receptor 2-independent innate immunity to Listeria: no role for either in macrophage listericidal activity. J Immunol. 169:2002;3869-3875.
    • (2002) J Immunol , vol.169 , pp. 3869-3875
    • Edelson, B.T.1    Unanue, E.R.2
  • 31
    • 0036785630 scopus 로고    scopus 로고
    • Critical roles of myeloid differentiation factor 88-dependent proinflammatory cytokine release in early phase clearance of Listeria monocytogenes in mice
    • Seki E., Tsutsui H., Tsuji N.M., Hayashi N., Adachi K., Nakano H., Futatsugi-Yumikura S., Takeuchi O., Hoshino K., Akira S.et al. Critical roles of myeloid differentiation factor 88-dependent proinflammatory cytokine release in early phase clearance of Listeria monocytogenes in mice. J Immunol. 169:2002;3863-3868.
    • (2002) J Immunol , vol.169 , pp. 3863-3868
    • Seki, E.1    Tsutsui, H.2    Tsuji, N.M.3    Hayashi, N.4    Adachi, K.5    Nakano, H.6    Futatsugi-Yumikura, S.7    Takeuchi, O.8    Hoshino, K.9    Akira, S.10
  • 32
    • 0034669910 scopus 로고    scopus 로고
    • Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection
    • Takeuchi O., Hoshino K., Akira S. Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection. J Immunol. 165:2000;5392-5396.
    • (2000) J Immunol , vol.165 , pp. 5392-5396
    • Takeuchi, O.1    Hoshino, K.2    Akira, S.3
  • 33
    • 0037097795 scopus 로고    scopus 로고
    • Cutting edge: MyD88 is required for resistance to Toxoplasma gondii infection and regulates parasite-induced IL-12 production by dendritic cells
    • Scanga C.A., Aliberti J., Jankovic D., Tilloy F., Bennouna S., Denkers E.Y., Medzhitov R., Sher A. Cutting edge: MyD88 is required for resistance to Toxoplasma gondii infection and regulates parasite-induced IL-12 production by dendritic cells. J Immunol. 168:2002;5997-6001.
    • (2002) J Immunol , vol.168 , pp. 5997-6001
    • Scanga, C.A.1    Aliberti, J.2    Jankovic, D.3    Tilloy, F.4    Bennouna, S.5    Denkers, E.Y.6    Medzhitov, R.7    Sher, A.8
  • 34
    • 0037105727 scopus 로고    scopus 로고
    • Toll-like receptor 2-deficient mice are highly susceptible to Streptococcus pneumoniae meningitis because of reduced bacterial clearing and enhanced inflammation
    • Echchannaoui H., Frei K., Schnell C., Leib S.L., Zimmerli W., Landmann R. Toll-like receptor 2-deficient mice are highly susceptible to Streptococcus pneumoniae meningitis because of reduced bacterial clearing and enhanced inflammation. J Infect Dis. 186:2002;798-806.
    • (2002) J Infect Dis , vol.186 , pp. 798-806
    • Echchannaoui, H.1    Frei, K.2    Schnell, C.3    Leib, S.L.4    Zimmerli, W.5    Landmann, R.6
  • 35
    • 0037220060 scopus 로고    scopus 로고
    • Toll-like receptor 2 participates in mediation of immune response in experimental pneumococcal meningitis
    • Koedel U., Angele B., Rupprecht T., Wagner H., Roggenkamp A., Pfister H.W., Kirschning C.J. Toll-like receptor 2 participates in mediation of immune response in experimental pneumococcal meningitis. J Immunol. 170:2003;438-444.
    • (2003) J Immunol , vol.170 , pp. 438-444
    • Koedel, U.1    Angele, B.2    Rupprecht, T.3    Wagner, H.4    Roggenkamp, A.5    Pfister, H.W.6    Kirschning, C.J.7
  • 36
    • 0036784614 scopus 로고    scopus 로고
    • Cutting edge: Toll-like receptor (TLR)2- and TLR4-mediated pathogen recognition in resistance to airborne infection with Mycobacterium tuberculosis
    • Reiling N., Holscher C., Fehrenbach A., Kroger S., Kirschning C.J., Goyert S., Ehlers S. Cutting edge: Toll-like receptor (TLR)2- and TLR4-mediated pathogen recognition in resistance to airborne infection with Mycobacterium tuberculosis. J Immunol. 169:2002;3480-3484.
    • (2002) J Immunol , vol.169 , pp. 3480-3484
    • Reiling, N.1    Holscher, C.2    Fehrenbach, A.3    Kroger, S.4    Kirschning, C.J.5    Goyert, S.6    Ehlers, S.7
  • 37
    • 0034891984 scopus 로고    scopus 로고
    • Detection of Toll-like receptor 2 (TLR2) mutation in the lepromatous leprosy patients
    • Kang T.J., Chae G.T. Detection of Toll-like receptor 2 (TLR2) mutation in the lepromatous leprosy patients. FEMS Immunol Med Microbiol. 31:2001;53-58.
    • (2001) FEMS Immunol Med Microbiol , vol.31 , pp. 53-58
    • Kang, T.J.1    Chae, G.T.2
  • 40
    • 0037080210 scopus 로고    scopus 로고
    • Toll-like receptor 4 mediates innate immune responses to Haemophilus influenzae infection in mouse lung
    • Wang X., Moser C., Louboutin J.-P., Lysenko E.S., Weiner D.J., Weiser J.N., Wilson J.M. Toll-like receptor 4 mediates innate immune responses to Haemophilus influenzae infection in mouse lung. J Immunol. 168:2002;810-815.
    • (2002) J Immunol , vol.168 , pp. 810-815
    • Wang, X.1    Moser, C.2    Louboutin, J.-P.3    Lysenko, E.S.4    Weiner, D.J.5    Weiser, J.N.6    Wilson, J.M.7
  • 42
    • 0037105425 scopus 로고    scopus 로고
    • Toll-like receptor 4 expression is required to control chronic Mycobacterium tuberculosis infection in mice
    • Abel B., Thieblemont N., Quesniaux V.J., Brown N., Mpagi J., Miyake K., Bihl F., Ryffel B. Toll-like receptor 4 expression is required to control chronic Mycobacterium tuberculosis infection in mice. J Immunol. 169:2002;3155-3162.
    • (2002) J Immunol , vol.169 , pp. 3155-3162
    • Abel, B.1    Thieblemont, N.2    Quesniaux, V.J.3    Brown, N.4    Mpagi, J.5    Miyake, K.6    Bihl, F.7    Ryffel, B.8
  • 45
  • 46
    • 0036838764 scopus 로고    scopus 로고
    • Respiratory syncytial virus-induced activation of nuclear factor-kappaB in the lung involves alveolar macrophages and toll-like receptor 4-dependent pathways
    • Haeberle H.A., Takizawa R., Casola A., Brasier A.R., Dieterich H.J., Van Rooijen N., Gatalica Z., Garofalo R.P. Respiratory syncytial virus-induced activation of nuclear factor-kappaB in the lung involves alveolar macrophages and toll-like receptor 4-dependent pathways. J Infect Dis. 186:2002;1199-1206.
    • (2002) J Infect Dis , vol.186 , pp. 1199-1206
    • Haeberle, H.A.1    Takizawa, R.2    Casola, A.3    Brasier, A.R.4    Dieterich, H.J.5    Van Rooijen, N.6    Gatalica, Z.7    Garofalo, R.P.8
  • 50
    • 0036222241 scopus 로고    scopus 로고
    • TLR4, but not TLR2, mediates IFN-beta-induced STAT1alpha/beta-dependent gene expression in macrophages
    • ••] identified that antiviral genes are induced by TLR3 and TLR4, but not by TLR2 or TLR9. By utilizing gene chip analysis, the authors discovered a broad set of genes dependent on NF-κB that are induced by apparently all four of these TLRs, and a subset of genes that are dependent on IRF3 that are induced by only TLR3 and TLR4
    • ••] identified that antiviral genes are induced by TLR3 and TLR4, but not by TLR2 or TLR9. By utilizing gene chip analysis, the authors discovered a broad set of genes dependent on NF-κB that are induced by apparently all four of these TLRs, and a subset of genes that are dependent on IRF3 that are induced by only TLR3 and TLR4.
    • (2002) Nat Immunol , vol.3 , pp. 392-398
    • Toshchakov, V.1    Jones, B.W.2    Perera, P.Y.3    Thomas, K.4    Cody, M.J.5    Zhang, S.6    Williams, B.R.7    Major, J.8    Hamilton, T.A.9    Fenton, M.J.10


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.