Defective interleukin (IL)-18-mediated natural killer and T helper cell type 1 responses in IL-1 receptor-associated kinase (IRAK)-deficient mice
Interleukin (IL)-18 is functionally similar to IL-12 in mediating T helper cell type 1 (Th1) response and natural killer (NK) cell activity but is related to IL-1 in protein structure and signaling, including recruitment of IL-1 receptor-associated kinase (IRAK) to the receptor and activation of c-J...
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| Veröffentlicht in: | The Journal of experimental medicine 1999-04, Vol.189 (7), p.1129-1138 |
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| container_title | The Journal of experimental medicine |
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| creator | Kanakaraj, P Ngo, K Wu, Y Angulo, A Ghazal, P Harris, C A Siekierka, J J Peterson, P A Fung-Leung, W P |
| description | Interleukin (IL)-18 is functionally similar to IL-12 in mediating T helper cell type 1 (Th1) response and natural killer (NK) cell activity but is related to IL-1 in protein structure and signaling, including recruitment of IL-1 receptor-associated kinase (IRAK) to the receptor and activation of c-Jun NH2-terminal kinase (JNK) and nuclear factor (NF)-kappaB. The role of IRAK in IL-18-induced responses was studied in IRAK-deficient mice. Significant defects in JNK induction and partial impairment in NF-kappaB activation were found in IRAK-deficient Th1 cells, resulting in a dramatic decrease in interferon (IFN)-gamma mRNA expression. In vivo Th1 response to Propionibacterium acnes and lipopolysaccharide in IFN-gamma production and induction of NK cytotoxicity by IL-18 were severely impaired in IRAK-deficient mice. IFN-gamma production by activated NK cells in an acute murine cytomegalovirus infection was significantly reduced despite normal induction of NK cytotoxicity. These results demonstrate that IRAK plays an important role in IL-18-induced signaling and function. |
| doi_str_mv | 10.1084/jem.189.7.1129 |
| format | Article |
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The role of IRAK in IL-18-induced responses was studied in IRAK-deficient mice. Significant defects in JNK induction and partial impairment in NF-kappaB activation were found in IRAK-deficient Th1 cells, resulting in a dramatic decrease in interferon (IFN)-gamma mRNA expression. In vivo Th1 response to Propionibacterium acnes and lipopolysaccharide in IFN-gamma production and induction of NK cytotoxicity by IL-18 were severely impaired in IRAK-deficient mice. IFN-gamma production by activated NK cells in an acute murine cytomegalovirus infection was significantly reduced despite normal induction of NK cytotoxicity. These results demonstrate that IRAK plays an important role in IL-18-induced signaling and function.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.189.7.1129</identifier><identifier>PMID: 10190904</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>AIDS/HIV ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases - biosynthesis ; Calcium-Calmodulin-Dependent Protein Kinases - genetics ; Cell Differentiation - drug effects ; Cell Division - drug effects ; Chimera ; Crosses, Genetic ; Cytomegalovirus Infections - immunology ; Cytotoxicity, Immunologic - drug effects ; Depression, Chemical ; Enzyme Activation - drug effects ; Enzyme Induction - drug effects ; Female ; Gene Expression Regulation - drug effects ; Interferon-gamma - biosynthesis ; Interferon-gamma - genetics ; Interleukin-1 Receptor-Associated Kinases ; Interleukin-18 - pharmacology ; Interleukin-18 Receptor alpha Subunit ; Interleukin-4 - biosynthesis ; Interleukin-4 - genetics ; JNK Mitogen-Activated Protein Kinases ; Killer Cells, Natural - immunology ; Lipopolysaccharides - immunology ; Lymphocyte Activation - drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitogen-Activated Protein Kinases ; NF-kappa B - metabolism ; Propionibacterium acnes - immunology ; Protein Kinases - deficiency ; Protein Kinases - genetics ; Protein Kinases - physiology ; Receptors, Interleukin - physiology ; Receptors, Interleukin-18 ; Signal Transduction - physiology ; Th1 Cells - cytology ; Th1 Cells - immunology ; Th2 Cells - cytology ; Th2 Cells - immunology</subject><ispartof>The Journal of experimental medicine, 1999-04, Vol.189 (7), p.1129-1138</ispartof><rights>1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-30225c08746ecbe78a653e3afc1d22add5aabd83dea6b037665579c5ece61dca3</citedby><cites>FETCH-LOGICAL-c386t-30225c08746ecbe78a653e3afc1d22add5aabd83dea6b037665579c5ece61dca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10190904$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kanakaraj, P</creatorcontrib><creatorcontrib>Ngo, K</creatorcontrib><creatorcontrib>Wu, Y</creatorcontrib><creatorcontrib>Angulo, A</creatorcontrib><creatorcontrib>Ghazal, P</creatorcontrib><creatorcontrib>Harris, C A</creatorcontrib><creatorcontrib>Siekierka, J J</creatorcontrib><creatorcontrib>Peterson, P A</creatorcontrib><creatorcontrib>Fung-Leung, W P</creatorcontrib><title>Defective interleukin (IL)-18-mediated natural killer and T helper cell type 1 responses in IL-1 receptor-associated kinase (IRAK)-deficient mice</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>Interleukin (IL)-18 is functionally similar to IL-12 in mediating T helper cell type 1 (Th1) response and natural killer (NK) cell activity but is related to IL-1 in protein structure and signaling, including recruitment of IL-1 receptor-associated kinase (IRAK) to the receptor and activation of c-Jun NH2-terminal kinase (JNK) and nuclear factor (NF)-kappaB. The role of IRAK in IL-18-induced responses was studied in IRAK-deficient mice. Significant defects in JNK induction and partial impairment in NF-kappaB activation were found in IRAK-deficient Th1 cells, resulting in a dramatic decrease in interferon (IFN)-gamma mRNA expression. In vivo Th1 response to Propionibacterium acnes and lipopolysaccharide in IFN-gamma production and induction of NK cytotoxicity by IL-18 were severely impaired in IRAK-deficient mice. IFN-gamma production by activated NK cells in an acute murine cytomegalovirus infection was significantly reduced despite normal induction of NK cytotoxicity. These results demonstrate that IRAK plays an important role in IL-18-induced signaling and function.</description><subject>AIDS/HIV</subject><subject>Animals</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - biosynthesis</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - genetics</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Chimera</subject><subject>Crosses, Genetic</subject><subject>Cytomegalovirus Infections - immunology</subject><subject>Cytotoxicity, Immunologic - drug effects</subject><subject>Depression, Chemical</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Induction - drug effects</subject><subject>Female</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interferon-gamma - genetics</subject><subject>Interleukin-1 Receptor-Associated Kinases</subject><subject>Interleukin-18 - pharmacology</subject><subject>Interleukin-18 Receptor alpha Subunit</subject><subject>Interleukin-4 - biosynthesis</subject><subject>Interleukin-4 - genetics</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>Killer Cells, Natural - immunology</subject><subject>Lipopolysaccharides - immunology</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mitogen-Activated Protein Kinases</subject><subject>NF-kappa B - metabolism</subject><subject>Propionibacterium acnes - immunology</subject><subject>Protein Kinases - deficiency</subject><subject>Protein Kinases - genetics</subject><subject>Protein Kinases - physiology</subject><subject>Receptors, Interleukin - physiology</subject><subject>Receptors, Interleukin-18</subject><subject>Signal Transduction - physiology</subject><subject>Th1 Cells - cytology</subject><subject>Th1 Cells - immunology</subject><subject>Th2 Cells - cytology</subject><subject>Th2 Cells - immunology</subject><issn>0022-1007</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1P3DAQtaqiskCvPVY-VeXg1I5jJ7lUQrTAqitVquBszdqTYshXbQeJn8E_rleLEJys8bx5b948Qj4JXgjeVN_ucChE0xZ1IUTZviMroSrOWiWb92TFeVkywXl9SI5ivONcVJXSH8ih4KLlLa9W5OkHdmiTf0Dqx4Shx-Xej_TrenPKRMMGdB4SOjpCWgL09N73PQYKo6PX9Bb7ORcW-56mxxmpoAHjPI0RY6aj6w3b_Vic0xQYxDjZPVuWgIhZ5c_Zr1PmsPPW45jo4C2ekIMO-ogfn99jcnPx8_r8im1-X67PzzbMykYnJrM3ZXlTVxrtFusGtJIoobPClSU4pwC2rpEOQW-5rLVWqm6tytto4SzIY_J9zzsv22zTZv1s0MzBDxAezQTevO2M_tb8nR5MKVqZb5oJvjwThOnfgjGZwcfdLWDEaYlGt7rWGZmBxR5owxRjwO5FRHCzS9HkFE1O0dRml2Ie-Px6tVfwfWzyP6OwmuM</recordid><startdate>19990405</startdate><enddate>19990405</enddate><creator>Kanakaraj, P</creator><creator>Ngo, K</creator><creator>Wu, Y</creator><creator>Angulo, A</creator><creator>Ghazal, P</creator><creator>Harris, C A</creator><creator>Siekierka, J J</creator><creator>Peterson, P A</creator><creator>Fung-Leung, W P</creator><general>The Rockefeller University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19990405</creationdate><title>Defective interleukin (IL)-18-mediated natural killer and T helper cell type 1 responses in IL-1 receptor-associated kinase (IRAK)-deficient mice</title><author>Kanakaraj, P ; Ngo, K ; Wu, Y ; Angulo, A ; Ghazal, P ; Harris, C A ; Siekierka, J J ; Peterson, P A ; Fung-Leung, W P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-30225c08746ecbe78a653e3afc1d22add5aabd83dea6b037665579c5ece61dca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>AIDS/HIV</topic><topic>Animals</topic><topic>Calcium-Calmodulin-Dependent Protein Kinases - biosynthesis</topic><topic>Calcium-Calmodulin-Dependent Protein Kinases - genetics</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Division - drug effects</topic><topic>Chimera</topic><topic>Crosses, Genetic</topic><topic>Cytomegalovirus Infections - immunology</topic><topic>Cytotoxicity, Immunologic - drug effects</topic><topic>Depression, Chemical</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Induction - drug effects</topic><topic>Female</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interferon-gamma - genetics</topic><topic>Interleukin-1 Receptor-Associated Kinases</topic><topic>Interleukin-18 - pharmacology</topic><topic>Interleukin-18 Receptor alpha Subunit</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Interleukin-4 - genetics</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>Killer Cells, Natural - immunology</topic><topic>Lipopolysaccharides - immunology</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mitogen-Activated Protein Kinases</topic><topic>NF-kappa B - metabolism</topic><topic>Propionibacterium acnes - immunology</topic><topic>Protein Kinases - deficiency</topic><topic>Protein Kinases - genetics</topic><topic>Protein Kinases - physiology</topic><topic>Receptors, Interleukin - physiology</topic><topic>Receptors, Interleukin-18</topic><topic>Signal Transduction - physiology</topic><topic>Th1 Cells - cytology</topic><topic>Th1 Cells - immunology</topic><topic>Th2 Cells - cytology</topic><topic>Th2 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kanakaraj, P</creatorcontrib><creatorcontrib>Ngo, K</creatorcontrib><creatorcontrib>Wu, Y</creatorcontrib><creatorcontrib>Angulo, A</creatorcontrib><creatorcontrib>Ghazal, P</creatorcontrib><creatorcontrib>Harris, C A</creatorcontrib><creatorcontrib>Siekierka, J J</creatorcontrib><creatorcontrib>Peterson, P A</creatorcontrib><creatorcontrib>Fung-Leung, W P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanakaraj, P</au><au>Ngo, K</au><au>Wu, Y</au><au>Angulo, A</au><au>Ghazal, P</au><au>Harris, C A</au><au>Siekierka, J J</au><au>Peterson, P A</au><au>Fung-Leung, W P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defective interleukin (IL)-18-mediated natural killer and T helper cell type 1 responses in IL-1 receptor-associated kinase (IRAK)-deficient mice</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>1999-04-05</date><risdate>1999</risdate><volume>189</volume><issue>7</issue><spage>1129</spage><epage>1138</epage><pages>1129-1138</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><abstract>Interleukin (IL)-18 is functionally similar to IL-12 in mediating T helper cell type 1 (Th1) response and natural killer (NK) cell activity but is related to IL-1 in protein structure and signaling, including recruitment of IL-1 receptor-associated kinase (IRAK) to the receptor and activation of c-Jun NH2-terminal kinase (JNK) and nuclear factor (NF)-kappaB. The role of IRAK in IL-18-induced responses was studied in IRAK-deficient mice. Significant defects in JNK induction and partial impairment in NF-kappaB activation were found in IRAK-deficient Th1 cells, resulting in a dramatic decrease in interferon (IFN)-gamma mRNA expression. In vivo Th1 response to Propionibacterium acnes and lipopolysaccharide in IFN-gamma production and induction of NK cytotoxicity by IL-18 were severely impaired in IRAK-deficient mice. IFN-gamma production by activated NK cells in an acute murine cytomegalovirus infection was significantly reduced despite normal induction of NK cytotoxicity. These results demonstrate that IRAK plays an important role in IL-18-induced signaling and function.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>10190904</pmid><doi>10.1084/jem.189.7.1129</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of experimental medicine, 1999-04, Vol.189 (7), p.1129-1138 |
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| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2193007 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | AIDS/HIV Animals Calcium-Calmodulin-Dependent Protein Kinases - biosynthesis Calcium-Calmodulin-Dependent Protein Kinases - genetics Cell Differentiation - drug effects Cell Division - drug effects Chimera Crosses, Genetic Cytomegalovirus Infections - immunology Cytotoxicity, Immunologic - drug effects Depression, Chemical Enzyme Activation - drug effects Enzyme Induction - drug effects Female Gene Expression Regulation - drug effects Interferon-gamma - biosynthesis Interferon-gamma - genetics Interleukin-1 Receptor-Associated Kinases Interleukin-18 - pharmacology Interleukin-18 Receptor alpha Subunit Interleukin-4 - biosynthesis Interleukin-4 - genetics JNK Mitogen-Activated Protein Kinases Killer Cells, Natural - immunology Lipopolysaccharides - immunology Lymphocyte Activation - drug effects Male Mice Mice, Inbred C57BL Mice, Knockout Mitogen-Activated Protein Kinases NF-kappa B - metabolism Propionibacterium acnes - immunology Protein Kinases - deficiency Protein Kinases - genetics Protein Kinases - physiology Receptors, Interleukin - physiology Receptors, Interleukin-18 Signal Transduction - physiology Th1 Cells - cytology Th1 Cells - immunology Th2 Cells - cytology Th2 Cells - immunology |
| title | 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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