IL-6 signal transduction and its physiological roles: the signal orchestration model
Identifieur interne : 001213 ( Main/Corpus ); précédent : 001212; suivant : 001214IL-6 signal transduction and its physiological roles: the signal orchestration model
Auteurs : D. Kamimura ; K. Ishihara ; T. HiranoSource :
- Reviews of Physiology, Biochemistry and Pharmacology [ 0303-4240 ] ; 2004.
Abstract
Abstract: Interleukin (IL)-6 is a pleiotropic cytokine that not only affects the immune system, but also acts in other biological systems and many physiological events in various organs. In a target cell, IL-6 can simultaneously generate functionally distinct or sometimes contradictory signals through its receptor complex, IL-6Rα and gp130. One good illustration is derived from the in vitro observations that IL-6 promotes the growth arrest and differentiation of M1 cells through gp130-mediated STAT3 activation, whereas the Y759/SHP-2-mediated cascade by gp130 stimulation has growth-enhancing effects. The final physiological output can be thought of as a consequence of the orchestration of the diverse signaling pathways generated by a given ligand. This concept, the signal orchestration model, may explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances. Elucidation of the molecular mechanisms underlying this issue is a challenging subject for future research. Intriguingly, recent in vivo studies indicated that the SHP-2-binding site- and YXXQ-mediated pathways through gp130 are not mutually exclusive but affect each other: a mutation at the SHP-2-binding site prolongs STAT3 activation, and a loss of STAT activation by gp130 truncation leads to sustained SHP-2/ERK MAPK phosphorylation. Although IL-6/gp130 signaling is a promising target for drug discovery for many human diseases, the interdependence of each signaling pathway may be an obstacle to the development of a nonpeptide orally active small molecule to inhibit one of these IL-6 signaling cascades, because it would disturb the signal orchestration. In mice, a consequence of the imbalanced signals causes unexpected results such as gastrointestinal disorders, autoimmune diseases, and/or chronic inflammatory proliferative diseases. However, lessons learned from IL-6 KO mice indicate that IL-6 is not essential for vital biological processes, but a significant impact on disease progression in many experimental models for human disorders. Thus, IL-6/gp130 signaling will become a more attractive therapeutic target for human inflammatory diseases when a better understanding of IL-6 signaling, including the identification of the conductor for gp130 signal transduction, is achieved.
Url:
DOI: 10.1007/s10254-003-0012-2
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">IL-6 signal transduction and its physiological roles: the signal orchestration model</title><author><name sortKey="Kamimura, D" sort="Kamimura, D" uniqKey="Kamimura D" first="D." last="Kamimura">D. Kamimura</name><affiliation><mods:affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ishihara, K" sort="Ishihara, K" uniqKey="Ishihara K" first="K." last="Ishihara">K. Ishihara</name><affiliation><mods:affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hirano, T" sort="Hirano, T" uniqKey="Hirano T" first="T." last="Hirano">T. Hirano</name><affiliation><mods:affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: hirano@molonc.med.osaka-u.ac.jp</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:E476EA2C956E949A5D7F514ACA1BF3F61A2ABC1D</idno><date when="2003" year="2003">2003</date><idno type="doi">10.1007/s10254-003-0012-2</idno><idno type="url">https://api.istex.fr/document/E476EA2C956E949A5D7F514ACA1BF3F61A2ABC1D/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001213</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">IL-6 signal transduction and its physiological roles: the signal orchestration model</title><author><name sortKey="Kamimura, D" sort="Kamimura, D" uniqKey="Kamimura D" first="D." last="Kamimura">D. Kamimura</name><affiliation><mods:affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ishihara, K" sort="Ishihara, K" uniqKey="Ishihara K" first="K." last="Ishihara">K. Ishihara</name><affiliation><mods:affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hirano, T" sort="Hirano, T" uniqKey="Hirano T" first="T." last="Hirano">T. Hirano</name><affiliation><mods:affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: hirano@molonc.med.osaka-u.ac.jp</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="s">Reviews of Physiology, Biochemistry and Pharmacology</title><imprint><date>2004</date></imprint><idno type="ISSN">0303-4240</idno><idno type="ISSN">0303-4240</idno></series><idno type="istex">E476EA2C956E949A5D7F514ACA1BF3F61A2ABC1D</idno><idno type="DOI">10.1007/s10254-003-0012-2</idno><idno type="ChapterID">Chap1</idno><idno type="ChapterID">1</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0303-4240</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Interleukin (IL)-6 is a pleiotropic cytokine that not only affects the immune system, but also acts in other biological systems and many physiological events in various organs. In a target cell, IL-6 can simultaneously generate functionally distinct or sometimes contradictory signals through its receptor complex, IL-6Rα and gp130. One good illustration is derived from the in vitro observations that IL-6 promotes the growth arrest and differentiation of M1 cells through gp130-mediated STAT3 activation, whereas the Y759/SHP-2-mediated cascade by gp130 stimulation has growth-enhancing effects. The final physiological output can be thought of as a consequence of the orchestration of the diverse signaling pathways generated by a given ligand. This concept, the signal orchestration model, may explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances. Elucidation of the molecular mechanisms underlying this issue is a challenging subject for future research. Intriguingly, recent in vivo studies indicated that the SHP-2-binding site- and YXXQ-mediated pathways through gp130 are not mutually exclusive but affect each other: a mutation at the SHP-2-binding site prolongs STAT3 activation, and a loss of STAT activation by gp130 truncation leads to sustained SHP-2/ERK MAPK phosphorylation. Although IL-6/gp130 signaling is a promising target for drug discovery for many human diseases, the interdependence of each signaling pathway may be an obstacle to the development of a nonpeptide orally active small molecule to inhibit one of these IL-6 signaling cascades, because it would disturb the signal orchestration. In mice, a consequence of the imbalanced signals causes unexpected results such as gastrointestinal disorders, autoimmune diseases, and/or chronic inflammatory proliferative diseases. However, lessons learned from IL-6 KO mice indicate that IL-6 is not essential for vital biological processes, but a significant impact on disease progression in many experimental models for human disorders. Thus, IL-6/gp130 signaling will become a more attractive therapeutic target for human inflammatory diseases when a better understanding of IL-6 signaling, including the identification of the conductor for gp130 signal transduction, is achieved.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>D. Kamimura</name><affiliations><json:string>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</json:string></affiliations></json:item><json:item><name>K. Ishihara</name><affiliations><json:string>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</json:string><json:string>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</json:string></affiliations></json:item><json:item><name>T. Hirano</name><affiliations><json:string>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</json:string><json:string>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</json:string><json:string>Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan</json:string><json:string>E-mail: hirano@molonc.med.osaka-u.ac.jp</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>Abstract: Interleukin (IL)-6 is a pleiotropic cytokine that not only affects the immune system, but also acts in other biological systems and many physiological events in various organs. In a target cell, IL-6 can simultaneously generate functionally distinct or sometimes contradictory signals through its receptor complex, IL-6Rα and gp130. One good illustration is derived from the in vitro observations that IL-6 promotes the growth arrest and differentiation of M1 cells through gp130-mediated STAT3 activation, whereas the Y759/SHP-2-mediated cascade by gp130 stimulation has growth-enhancing effects. The final physiological output can be thought of as a consequence of the orchestration of the diverse signaling pathways generated by a given ligand. This concept, the signal orchestration model, may explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances. Elucidation of the molecular mechanisms underlying this issue is a challenging subject for future research. Intriguingly, recent in vivo studies indicated that the SHP-2-binding site- and YXXQ-mediated pathways through gp130 are not mutually exclusive but affect each other: a mutation at the SHP-2-binding site prolongs STAT3 activation, and a loss of STAT activation by gp130 truncation leads to sustained SHP-2/ERK MAPK phosphorylation. Although IL-6/gp130 signaling is a promising target for drug discovery for many human diseases, the interdependence of each signaling pathway may be an obstacle to the development of a nonpeptide orally active small molecule to inhibit one of these IL-6 signaling cascades, because it would disturb the signal orchestration. In mice, a consequence of the imbalanced signals causes unexpected results such as gastrointestinal disorders, autoimmune diseases, and/or chronic inflammatory proliferative diseases. However, lessons learned from IL-6 KO mice indicate that IL-6 is not essential for vital biological processes, but a significant impact on disease progression in many experimental models for human disorders. Thus, IL-6/gp130 signaling will become a more attractive therapeutic target for human inflammatory diseases when a better understanding of IL-6 signaling, including the identification of the conductor for gp130 signal transduction, is achieved.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>437 x 666 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>2337</abstractCharCount><pdfWordCount>18962</pdfWordCount><pdfCharCount>115537</pdfCharCount><pdfPageCount>38</pdfPageCount><abstractWordCount>328</abstractWordCount></qualityIndicators><title>IL-6 signal transduction and its physiological roles: the signal orchestration model</title><genre><json:string>Book Chapter</json:string></genre><serie><editor><json:item><name>S. G. Amara</name><affiliations><json:string>Protland</json:string></affiliations></json:item><json:item><name>E. 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physiological events in various organs. In a target cell, IL-6 can simultaneously generate functionally distinct or sometimes contradictory signals through its receptor complex, IL-6Rα and gp130. One good illustration is derived from the in vitro observations that IL-6 promotes the growth arrest and differentiation of M1 cells through gp130-mediated STAT3 activation, whereas the Y759/SHP-2-mediated cascade by gp130 stimulation has growth-enhancing effects. The final physiological output can be thought of as a consequence of the orchestration of the diverse signaling pathways generated by a given ligand. This concept, the signal orchestration model, may explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances. Elucidation of the molecular mechanisms underlying this issue is a challenging subject for future research. Intriguingly, recent in vivo studies indicated that the SHP-2-binding site- and YXXQ-mediated pathways through gp130 are not mutually exclusive but affect each other: a mutation at the SHP-2-binding site prolongs STAT3 activation, and a loss of STAT activation by gp130 truncation leads to sustained SHP-2/ERK MAPK phosphorylation. Although IL-6/gp130 signaling is a promising target for drug discovery for many human diseases, the interdependence of each signaling pathway may be an obstacle to the development of a nonpeptide orally active small molecule to inhibit one of these IL-6 signaling cascades, because it would disturb the signal orchestration. In mice, a consequence of the imbalanced signals causes unexpected results such as gastrointestinal disorders, autoimmune diseases, and/or chronic inflammatory proliferative diseases. However, lessons learned from IL-6 KO mice indicate that IL-6 is not essential for vital biological processes, but a significant impact on disease progression in many experimental models for human disorders. Thus, IL-6/gp130 signaling will become a more attractive therapeutic target for human inflammatory diseases when a better understanding of IL-6 signaling, including the identification of the conductor for gp130 signal transduction, is achieved.</p></abstract><textClass><keywords scheme="Book Subject Collection"><list><label>SUCO11642</label><item><term>Biomedical and Life Sciences</term></item></list></keywords></textClass><textClass><keywords scheme="Book Subject Group"><list><label>B</label><label>B0000X</label><item><term>Biomedicine</term></item><item><term>Biomedicine general</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References 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BookProductType="Monograph" Language="En" MediaType="eBook" NumberingStyle="Unnumbered" TocLevels="0"><BookID>978-3-540-45205-8</BookID><BookTitle>Reviews of Physiology, Biochemistry and Pharmacology</BookTitle><BookVolumeNumber>149</BookVolumeNumber><BookSequenceNumber>149</BookSequenceNumber><BookDOI>10.1007/978-3-540-45205-8</BookDOI><BookTitleID>80251</BookTitleID><BookPrintISBN>978-3-540-20213-4</BookPrintISBN><BookElectronicISBN>978-3-540-45205-8</BookElectronicISBN><BookChapterCount>5</BookChapterCount><BookHistory><OnlineDate><Year>2003</Year><Month>10</Month><Day>30</Day></OnlineDate></BookHistory><BookCopyright><CopyrightHolderName>Springer-Verlag Berlin Heidelberg</CopyrightHolderName><CopyrightYear>2004</CopyrightYear></BookCopyright><BookSubjectGroup><BookSubject Code="B" Type="Primary">Biomedicine</BookSubject><BookSubject Code="B0000X" Priority="1" Type="Secondary">Biomedicine general</BookSubject><SubjectCollection Code="SUCO11642">Biomedical and Life Sciences</SubjectCollection></BookSubjectGroup></BookInfo><Chapter ID="Chap1" Language="En"><ChapterInfo ChapterType="OriginalPaper" ContainsESM="No" NumberingStyle="Unnumbered" TocLevels="0"><ChapterID>1</ChapterID><ChapterDOI>10.1007/s10254-003-0012-2</ChapterDOI><ChapterSequenceNumber>1</ChapterSequenceNumber><ChapterTitle Language="En">IL-6 signal transduction and its physiological roles: the signal orchestration model</ChapterTitle><ChapterFirstPage>1</ChapterFirstPage><ChapterLastPage>38</ChapterLastPage><ChapterCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>2003</CopyrightYear></ChapterCopyright><ChapterHistory><RegistrationDate><Year>2003</Year><Month>10</Month><Day>30</Day></RegistrationDate><OnlineDate><Year>2003</Year><Month>10</Month><Day>29</Day></OnlineDate></ChapterHistory><ChapterGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ChapterGrants><ChapterContext><SeriesID>112</SeriesID><BookID>978-3-540-45205-8</BookID><BookTitle>Reviews of Physiology, Biochemistry and Pharmacology</BookTitle></ChapterContext></ChapterInfo><ChapterHeader><AuthorGroup><Author AffiliationIDS="Aff11"><AuthorName DisplayOrder="Western"><GivenName>D.</GivenName><FamilyName>Kamimura</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff11 Aff12"><AuthorName DisplayOrder="Western"><GivenName>K.</GivenName><FamilyName>Ishihara</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff11 Aff12 Aff13" CorrespondingAffiliationID="Aff11"><AuthorName DisplayOrder="Western"><GivenName>T.</GivenName><FamilyName>Hirano</FamilyName></AuthorName><Contact><Fax>+81-6-68793889</Fax><Email>hirano@molonc.med.osaka-u.ac.jp</Email></Contact></Author><Affiliation ID="Aff11"><OrgDivision>Department of Molecular Oncology, Graduate School of Medicine</OrgDivision><OrgName>Osaka University</OrgName><OrgAddress><City>Suita, Osaka</City><Country>Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff12"><OrgDivision>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences</OrgDivision><OrgName>Osaka University</OrgName><OrgAddress><City>Osaka</City><Country>Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff13"><OrgDivision>Laboratory for Cytokine Signaling</OrgDivision><OrgName>RIKEN Research Center for Allergy and Immunology</OrgName><OrgAddress><City>Yokohama</City><Country>Japan</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>Interleukin (IL)-6 is a pleiotropic cytokine that not only affects the immune system, but also acts in other biological systems and many physiological events in various organs. In a target cell, IL-6 can simultaneously generate functionally distinct or sometimes contradictory signals through its receptor complex, IL-6Rα and gp130. One good illustration is derived from the in vitro observations that IL-6 promotes the growth arrest and differentiation of M1 cells through gp130-mediated STAT3 activation, whereas the Y759/SHP-2-mediated cascade by gp130 stimulation has growth-enhancing effects. The final physiological output can be thought of as a consequence of the orchestration of the diverse signaling pathways generated by a given ligand. This concept, <Emphasis Type="Italic">the signal orchestration model</Emphasis>, may explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances. Elucidation of the molecular mechanisms underlying this issue is a challenging subject for future research. Intriguingly, recent in vivo studies indicated that the SHP-2-binding site- and YXXQ-mediated pathways through gp130 are not mutually exclusive but affect each other: a mutation at the SHP-2-binding site prolongs STAT3 activation, and a loss of STAT activation by gp130 truncation leads to sustained SHP-2/ERK MAPK phosphorylation. Although IL-6/gp130 signaling is a promising target for drug discovery for many human diseases, the interdependence of each signaling pathway may be an obstacle to the development of a nonpeptide orally active small molecule to inhibit one of these IL-6 signaling cascades, because it would disturb the signal orchestration. In mice, a consequence of the imbalanced signals causes unexpected results such as gastrointestinal disorders, autoimmune diseases, and/or chronic inflammatory proliferative diseases. However, lessons learned from IL-6 KO mice indicate that IL-6 is not essential for vital biological processes, but a significant impact on disease progression in many experimental models for human disorders. Thus, IL-6/gp130 signaling will become a more attractive therapeutic target for human inflammatory diseases when a better understanding of IL-6 signaling, including the identification of <Emphasis Type="Italic">the conductor</Emphasis> for gp130 signal transduction, is achieved.</Para></Abstract></ChapterHeader><NoBody></NoBody></Chapter></Book></Series></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>IL-6 signal transduction and its physiological roles: the signal orchestration model</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>IL-6 signal transduction and its physiological roles: the signal orchestration model</title></titleInfo><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Kamimura</namePart><affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Ishihara</namePart><affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</affiliation><affiliation>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">T.</namePart><namePart type="family">Hirano</namePart><affiliation>Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan</affiliation><affiliation>Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan</affiliation><affiliation>Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan</affiliation><affiliation>E-mail: hirano@molonc.med.osaka-u.ac.jp</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer Berlin Heidelberg</publisher><place><placeTerm type="text">Berlin, Heidelberg</placeTerm></place><dateIssued encoding="w3cdtf">2003</dateIssued><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Abstract: Interleukin (IL)-6 is a pleiotropic cytokine that not only affects the immune system, but also acts in other biological systems and many physiological events in various organs. In a target cell, IL-6 can simultaneously generate functionally distinct or sometimes contradictory signals through its receptor complex, IL-6Rα and gp130. One good illustration is derived from the in vitro observations that IL-6 promotes the growth arrest and differentiation of M1 cells through gp130-mediated STAT3 activation, whereas the Y759/SHP-2-mediated cascade by gp130 stimulation has growth-enhancing effects. The final physiological output can be thought of as a consequence of the orchestration of the diverse signaling pathways generated by a given ligand. This concept, the signal orchestration model, may explain how IL-6 can elicit proinflammatory or anti-inflammatory effects, depending on the in vivo environmental circumstances. Elucidation of the molecular mechanisms underlying this issue is a challenging subject for future research. Intriguingly, recent in vivo studies indicated that the SHP-2-binding site- and YXXQ-mediated pathways through gp130 are not mutually exclusive but affect each other: a mutation at the SHP-2-binding site prolongs STAT3 activation, and a loss of STAT activation by gp130 truncation leads to sustained SHP-2/ERK MAPK phosphorylation. Although IL-6/gp130 signaling is a promising target for drug discovery for many human diseases, the interdependence of each signaling pathway may be an obstacle to the development of a nonpeptide orally active small molecule to inhibit one of these IL-6 signaling cascades, because it would disturb the signal orchestration. In mice, a consequence of the imbalanced signals causes unexpected results such as gastrointestinal disorders, autoimmune diseases, and/or chronic inflammatory proliferative diseases. However, lessons learned from IL-6 KO mice indicate that IL-6 is not essential for vital biological processes, but a significant impact on disease progression in many experimental models for human disorders. Thus, IL-6/gp130 signaling will become a more attractive therapeutic target for human inflammatory diseases when a better understanding of IL-6 signaling, including the identification of the conductor for gp130 signal transduction, is achieved.</abstract><relatedItem type="host"><titleInfo><title>Reviews of Physiology, Biochemistry and Pharmacology</title></titleInfo><genre type="Book Series" displayLabel="Monograph"></genre><originInfo><copyrightDate encoding="w3cdtf">2004</copyrightDate><issuance>monographic</issuance></originInfo><subject><genre>Book Subject Collection</genre><topic authority="SpringerSubjectCodes" authorityURI="SUCO11642">Biomedical and Life Sciences</topic></subject><subject><genre>Book Subject Group</genre><topic authority="SpringerSubjectCodes" authorityURI="B">Biomedicine</topic><topic authority="SpringerSubjectCodes" authorityURI="B0000X">Biomedicine general</topic></subject><identifier type="DOI">10.1007/978-3-540-45205-8</identifier><identifier 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