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Expression of Epstein–Barr virus‐induced gene 3 and other interleukin‐12‐related molecules by human intestinal epithelium
Summary Antigen‐presenting cells, including dendritic cells, monocytes and macrophages, produce members of the interleukin‐12 (IL‐12) family that are important in initiating and maintaining cell‐mediated immune responses. These include IL‐12p35 and p19 that dimerize with IL‐12p40 to form IL‐12 (also...
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| Published in: | Immunology 2004-07, Vol.112 (3), p.437-445 |
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| container_end_page | 445 |
| container_issue | 3 |
| container_start_page | 437 |
| container_title | Immunology |
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| creator | Maaser, Christian Egan, Laurence J. Birkenbach, Mark P. Eckmann, Lars Kagnoff, Martin F. |
| description | Summary
Antigen‐presenting cells, including dendritic cells, monocytes and macrophages, produce members of the interleukin‐12 (IL‐12) family that are important in initiating and maintaining cell‐mediated immune responses. These include IL‐12p35 and p19 that dimerize with IL‐12p40 to form IL‐12 (also termed IL‐12p75) and IL‐23, respectively, and Epstein–Barr virus‐induced gene 3 (EBI3) protein (a protein related to IL‐12p40), that forms a dimer with p28, termed IL‐27. Intestinal epithelial cells, which are the initial site of contact between the host and enteric pathogens, can act as antigen‐presenting cells, and are known to express mediators important in inflammatory and immune responses. In the current studies, we hypothesized that intestinal epithelial cells express members of the IL‐12 family, which can function as an early signalling system important in mucosal immunity. Using in vitro and in vivo model systems of human intestinal epithelium, we demonstrate the regulated expression of EBI3, IL‐12p35 and p19 by human intestinal epithelial cells. However, intestinal epithelial cells do not coexpress IL‐12p40 or p28 that are required to generate heterodimeric IL‐12p75, IL‐23 and IL‐27. To the extent that IL‐12p35, p19 and EBI3 cannot form IL‐12p75, IL‐23 or IL‐27 heterodimers in intestinal epithelial cells, these data suggest that those cells may express other, currently unknown, molecules that can associate with EBI3, IL‐12p35 and/or p19 or, alternatively, intestinal epithelial cells may release IL‐12‐related molecules that by themselves, or in combination with other molecules in the mucosal microenvironment, mediate biological activities. |
| doi_str_mv | 10.1111/j.1365-2567.2004.01895.x |
| format | article |
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Antigen‐presenting cells, including dendritic cells, monocytes and macrophages, produce members of the interleukin‐12 (IL‐12) family that are important in initiating and maintaining cell‐mediated immune responses. These include IL‐12p35 and p19 that dimerize with IL‐12p40 to form IL‐12 (also termed IL‐12p75) and IL‐23, respectively, and Epstein–Barr virus‐induced gene 3 (EBI3) protein (a protein related to IL‐12p40), that forms a dimer with p28, termed IL‐27. Intestinal epithelial cells, which are the initial site of contact between the host and enteric pathogens, can act as antigen‐presenting cells, and are known to express mediators important in inflammatory and immune responses. In the current studies, we hypothesized that intestinal epithelial cells express members of the IL‐12 family, which can function as an early signalling system important in mucosal immunity. Using in vitro and in vivo model systems of human intestinal epithelium, we demonstrate the regulated expression of EBI3, IL‐12p35 and p19 by human intestinal epithelial cells. However, intestinal epithelial cells do not coexpress IL‐12p40 or p28 that are required to generate heterodimeric IL‐12p75, IL‐23 and IL‐27. To the extent that IL‐12p35, p19 and EBI3 cannot form IL‐12p75, IL‐23 or IL‐27 heterodimers in intestinal epithelial cells, these data suggest that those cells may express other, currently unknown, molecules that can associate with EBI3, IL‐12p35 and/or p19 or, alternatively, intestinal epithelial cells may release IL‐12‐related molecules that by themselves, or in combination with other molecules in the mucosal microenvironment, mediate biological activities.</description><identifier>ISSN: 0019-2805</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.1111/j.1365-2567.2004.01895.x</identifier><identifier>PMID: 15196212</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Cell Line ; Epithelial Cells - immunology ; Epstein-Barr virus ; Epstein–Barr virus‐induced gene‐3 ; Glycoproteins - analysis ; Glycoproteins - immunology ; Humans ; IL‐12p35 ; IL‐12‐related molecules ; Immunity, Mucosal ; Immunoblotting - methods ; Immunohistochemistry - methods ; Interleukin-12 - analysis ; Interleukin-12 - immunology ; Interleukins ; intestinal epithelial cells ; intestinal xenograft ; Intestines - immunology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Minor Histocompatibility Antigens ; Original ; p19 ; p28 ; Receptors, Cytokine - analysis ; Receptors, Cytokine - immunology ; Reverse Transcriptase Polymerase Chain Reaction ; Transplantation, Heterologous</subject><ispartof>Immunology, 2004-07, Vol.112 (3), p.437-445</ispartof><rights>Copyright Blackwell Scientific Publications Ltd. Jul 2004</rights><rights>2004 Blackwell Publishing Ltd 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6195-b760b80d05b27db196ad6e2e4e1dcba8c0769a05866f28868cabcfb715cbca273</citedby><cites>FETCH-LOGICAL-c6195-b760b80d05b27db196ad6e2e4e1dcba8c0769a05866f28868cabcfb715cbca273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2567.2004.01895.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2567.2004.01895.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,27957,27958,50923,51032,53827,53829</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15196212$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maaser, Christian</creatorcontrib><creatorcontrib>Egan, Laurence J.</creatorcontrib><creatorcontrib>Birkenbach, Mark P.</creatorcontrib><creatorcontrib>Eckmann, Lars</creatorcontrib><creatorcontrib>Kagnoff, Martin F.</creatorcontrib><title>Expression of Epstein–Barr virus‐induced gene 3 and other interleukin‐12‐related molecules by human intestinal epithelium</title><title>Immunology</title><addtitle>Immunology</addtitle><description>Summary
Antigen‐presenting cells, including dendritic cells, monocytes and macrophages, produce members of the interleukin‐12 (IL‐12) family that are important in initiating and maintaining cell‐mediated immune responses. These include IL‐12p35 and p19 that dimerize with IL‐12p40 to form IL‐12 (also termed IL‐12p75) and IL‐23, respectively, and Epstein–Barr virus‐induced gene 3 (EBI3) protein (a protein related to IL‐12p40), that forms a dimer with p28, termed IL‐27. Intestinal epithelial cells, which are the initial site of contact between the host and enteric pathogens, can act as antigen‐presenting cells, and are known to express mediators important in inflammatory and immune responses. In the current studies, we hypothesized that intestinal epithelial cells express members of the IL‐12 family, which can function as an early signalling system important in mucosal immunity. Using in vitro and in vivo model systems of human intestinal epithelium, we demonstrate the regulated expression of EBI3, IL‐12p35 and p19 by human intestinal epithelial cells. However, intestinal epithelial cells do not coexpress IL‐12p40 or p28 that are required to generate heterodimeric IL‐12p75, IL‐23 and IL‐27. To the extent that IL‐12p35, p19 and EBI3 cannot form IL‐12p75, IL‐23 or IL‐27 heterodimers in intestinal epithelial cells, these data suggest that those cells may express other, currently unknown, molecules that can associate with EBI3, IL‐12p35 and/or p19 or, alternatively, intestinal epithelial cells may release IL‐12‐related molecules that by themselves, or in combination with other molecules in the mucosal microenvironment, mediate biological activities.</description><subject>Animals</subject><subject>Cell Line</subject><subject>Epithelial Cells - immunology</subject><subject>Epstein-Barr virus</subject><subject>Epstein–Barr virus‐induced gene‐3</subject><subject>Glycoproteins - analysis</subject><subject>Glycoproteins - immunology</subject><subject>Humans</subject><subject>IL‐12p35</subject><subject>IL‐12‐related molecules</subject><subject>Immunity, Mucosal</subject><subject>Immunoblotting - methods</subject><subject>Immunohistochemistry - methods</subject><subject>Interleukin-12 - analysis</subject><subject>Interleukin-12 - immunology</subject><subject>Interleukins</subject><subject>intestinal epithelial cells</subject><subject>intestinal xenograft</subject><subject>Intestines - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, SCID</subject><subject>Minor Histocompatibility Antigens</subject><subject>Original</subject><subject>p19</subject><subject>p28</subject><subject>Receptors, Cytokine - analysis</subject><subject>Receptors, Cytokine - immunology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Transplantation, Heterologous</subject><issn>0019-2805</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqNks1u1DAQxyMEokvhFZDFgVuC7cSOcwCJVgtUasUFzpbjTLpeHHuxk7J7K29QiTfsk-B0V-XjAj74Q_Obv2b8nyxDBBckrVfrgpSc5ZTxuqAYVwUmomHF9kG2uA88zBYYkyanArOj7EmM6_QsMWOPsyPCSMMpoYvs-3K7CRCj8Q75Hi03cQTjbq9_nKgQ0JUJU7y9vjGumzR06BIcoBIp1yE_riAg40YIFqYvc84NoWkLYNWY2MFb0JOFiNodWk2Dcnd0HI1TFsHGJAFrpuFp9qhXNsKzw3mcfX63_HT6IT__-P7s9O15rjlpWN7WHLcCd5i1tO7aVL_qOFCogHS6VULjmjcKM8F5T4XgQqtW921NmG61onV5nL3Z626mdoBOgxuDsnITzKDCTnpl5J8RZ1by0l9JUgvKME0CLw8CwX-dUiNyMFGDtcqBn6KsKaaVYNU_QSKSXRXnCXzxF7j2U0jfk5imqUhVVzMk9pAOPsYA_X3JBMt5GuRazqbL2XQ5T4O8mwa5TanPf2_5V-LB_gS83gPfjIXdfwvLs4uL-Vb-BIUjyns</recordid><startdate>200407</startdate><enddate>200407</enddate><creator>Maaser, Christian</creator><creator>Egan, Laurence J.</creator><creator>Birkenbach, Mark P.</creator><creator>Eckmann, Lars</creator><creator>Kagnoff, Martin F.</creator><general>Blackwell Science Ltd</general><general>Wiley Subscription Services, Inc</general><general>Blackwell Science Inc</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>7QL</scope><scope>7QR</scope><scope>7T5</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200407</creationdate><title>Expression of Epstein–Barr virus‐induced gene 3 and other interleukin‐12‐related molecules by human intestinal epithelium</title><author>Maaser, Christian ; Egan, Laurence J. ; Birkenbach, Mark P. ; Eckmann, Lars ; Kagnoff, Martin F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6195-b760b80d05b27db196ad6e2e4e1dcba8c0769a05866f28868cabcfb715cbca273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Cell Line</topic><topic>Epithelial Cells - immunology</topic><topic>Epstein-Barr virus</topic><topic>Epstein–Barr virus‐induced gene‐3</topic><topic>Glycoproteins - analysis</topic><topic>Glycoproteins - immunology</topic><topic>Humans</topic><topic>IL‐12p35</topic><topic>IL‐12‐related molecules</topic><topic>Immunity, Mucosal</topic><topic>Immunoblotting - methods</topic><topic>Immunohistochemistry - methods</topic><topic>Interleukin-12 - analysis</topic><topic>Interleukin-12 - immunology</topic><topic>Interleukins</topic><topic>intestinal epithelial cells</topic><topic>intestinal xenograft</topic><topic>Intestines - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, SCID</topic><topic>Minor Histocompatibility Antigens</topic><topic>Original</topic><topic>p19</topic><topic>p28</topic><topic>Receptors, Cytokine - analysis</topic><topic>Receptors, Cytokine - immunology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Transplantation, Heterologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maaser, Christian</creatorcontrib><creatorcontrib>Egan, Laurence J.</creatorcontrib><creatorcontrib>Birkenbach, Mark P.</creatorcontrib><creatorcontrib>Eckmann, Lars</creatorcontrib><creatorcontrib>Kagnoff, Martin F.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maaser, Christian</au><au>Egan, Laurence J.</au><au>Birkenbach, Mark P.</au><au>Eckmann, Lars</au><au>Kagnoff, Martin F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of Epstein–Barr virus‐induced gene 3 and other interleukin‐12‐related molecules by human intestinal epithelium</atitle><jtitle>Immunology</jtitle><addtitle>Immunology</addtitle><date>2004-07</date><risdate>2004</risdate><volume>112</volume><issue>3</issue><spage>437</spage><epage>445</epage><pages>437-445</pages><issn>0019-2805</issn><eissn>1365-2567</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><notes>ObjectType-Article-1</notes><notes>ObjectType-Feature-2</notes><abstract>Summary
Antigen‐presenting cells, including dendritic cells, monocytes and macrophages, produce members of the interleukin‐12 (IL‐12) family that are important in initiating and maintaining cell‐mediated immune responses. These include IL‐12p35 and p19 that dimerize with IL‐12p40 to form IL‐12 (also termed IL‐12p75) and IL‐23, respectively, and Epstein–Barr virus‐induced gene 3 (EBI3) protein (a protein related to IL‐12p40), that forms a dimer with p28, termed IL‐27. Intestinal epithelial cells, which are the initial site of contact between the host and enteric pathogens, can act as antigen‐presenting cells, and are known to express mediators important in inflammatory and immune responses. In the current studies, we hypothesized that intestinal epithelial cells express members of the IL‐12 family, which can function as an early signalling system important in mucosal immunity. Using in vitro and in vivo model systems of human intestinal epithelium, we demonstrate the regulated expression of EBI3, IL‐12p35 and p19 by human intestinal epithelial cells. However, intestinal epithelial cells do not coexpress IL‐12p40 or p28 that are required to generate heterodimeric IL‐12p75, IL‐23 and IL‐27. To the extent that IL‐12p35, p19 and EBI3 cannot form IL‐12p75, IL‐23 or IL‐27 heterodimers in intestinal epithelial cells, these data suggest that those cells may express other, currently unknown, molecules that can associate with EBI3, IL‐12p35 and/or p19 or, alternatively, intestinal epithelial cells may release IL‐12‐related molecules that by themselves, or in combination with other molecules in the mucosal microenvironment, mediate biological activities.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15196212</pmid><doi>10.1111/j.1365-2567.2004.01895.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Line Epithelial Cells - immunology Epstein-Barr virus Epstein–Barr virus‐induced gene‐3 Glycoproteins - analysis Glycoproteins - immunology Humans IL‐12p35 IL‐12‐related molecules Immunity, Mucosal Immunoblotting - methods Immunohistochemistry - methods Interleukin-12 - analysis Interleukin-12 - immunology Interleukins intestinal epithelial cells intestinal xenograft Intestines - immunology Mice Mice, Inbred C57BL Mice, SCID Minor Histocompatibility Antigens Original p19 p28 Receptors, Cytokine - analysis Receptors, Cytokine - immunology Reverse Transcriptase Polymerase Chain Reaction Transplantation, Heterologous |
| title | Expression of Epstein–Barr virus‐induced gene 3 and other interleukin‐12‐related molecules by human intestinal epithelium |
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