Expression of IL33 and IL35 in oral lichen planus
Oral lichen planus (OLP) is a complex immunological disorder, mediated in part by the release of cytokines by activated T-cells. Recently, the role of novel cytokines including IL33 and IL35 has been described in various chronic inflammatory diseases. IL33, a member of the IL-1 superfamily of cytoki...
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| Veröffentlicht in: | Archives of Dermatological Research 2018-07, Vol.310 (5), p.431-441 |
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| description | Oral lichen planus (OLP) is a complex immunological disorder, mediated in part by the release of cytokines by activated T-cells. Recently, the role of novel cytokines including IL33 and IL35 has been described in various chronic inflammatory diseases. IL33, a member of the IL-1 superfamily of cytokines, functions as an ‘alarmin’ released after cell necrosis to alert the immune system to tissue damage or stress. IL35, a member of IL12 cytokine family, is produced by regulatory T-cells and suppresses the immune response. The expression of IL33 and IL35 is yet to be investigated in OLP. The aim of this study was to determine the presence and topographical distribution of IL33 and IL35 in OLP using immunohistochemistry and quantitative real-time reverse transcriptase polymerase chain reaction (qPCR). For IHC, formalin-fixed paraffin-embedded archival specimens of OLP (
n
= 10) and a non-specific inflammatory (NSI) control group (
n
= 9) were used. A double-labelling immunofluorescence technique was used to determine the expression of IL33 and IL35 on CD3
+
T-cells. In addition, 12 fresh tissue samples (OLP
n
= 6 and NSI controls
n
= 6) were used to determine the gene expression of IL33 and EBI3 (one chain of the dimeric IL35). Quantitative and qualitative analysis was performed with statistical significance set at
p
|
| doi_str_mv | 10.1007/s00403-018-1829-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2023730051</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2023262152</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-832aeadf90dff9c2d602e66fe2c1917473f447cc52fe1ea83650471446695aeb3</originalsourceid><addsrcrecordid>eNp1kE1LAzEQhoMottT-AC-y4MVLdPK9OUqpWih4UfAW0myiW7a7NemC_ntT1w8QzGVC5pk3w4PQKYFLAqCuEgAHhoGUmJRUY3GAxoQzikHqp0M0BsYBM6nlCE1TWkM-CjgFdYxGVEvGgIgxIvO3bfQp1V1bdKFYLBkrbFvtL6Ko81u0TdHU7sW3xbaxbZ9O0FGwTfLTrzpBjzfzh9kdXt7fLmbXS-yYojtcMmq9rYKGKgTtaCWBeimDp45oorhigXPlnKDBE29LJgVwRTiXUgvrV2yCLobcbexee592ZlMn55u8hO_6ZChQphiAIBk9_4Ouuz62ebtPikpKBM0UGSgXu5SiD2Yb642N74aA2Ss1g1KTlZq9UiPyzNlXcr_a-Opn4ltgBugApNxqn338_fr_1A8aa3zA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2023262152</pqid></control><display><type>article</type><title>Expression of IL33 and IL35 in oral lichen planus</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Javvadi, L. R. ; Parachuru, V. P. B. ; Milne, T. J. ; Seymour, G. J. ; Rich, Alison M.</creator><creatorcontrib>Javvadi, L. R. ; Parachuru, V. P. B. ; Milne, T. J. ; Seymour, G. J. ; Rich, Alison M.</creatorcontrib><description>Oral lichen planus (OLP) is a complex immunological disorder, mediated in part by the release of cytokines by activated T-cells. Recently, the role of novel cytokines including IL33 and IL35 has been described in various chronic inflammatory diseases. IL33, a member of the IL-1 superfamily of cytokines, functions as an ‘alarmin’ released after cell necrosis to alert the immune system to tissue damage or stress. IL35, a member of IL12 cytokine family, is produced by regulatory T-cells and suppresses the immune response. The expression of IL33 and IL35 is yet to be investigated in OLP. The aim of this study was to determine the presence and topographical distribution of IL33 and IL35 in OLP using immunohistochemistry and quantitative real-time reverse transcriptase polymerase chain reaction (qPCR). For IHC, formalin-fixed paraffin-embedded archival specimens of OLP (
n
= 10) and a non-specific inflammatory (NSI) control group (
n
= 9) were used. A double-labelling immunofluorescence technique was used to determine the expression of IL33 and IL35 on CD3
+
T-cells. In addition, 12 fresh tissue samples (OLP
n
= 6 and NSI controls
n
= 6) were used to determine the gene expression of IL33 and EBI3 (one chain of the dimeric IL35). Quantitative and qualitative analysis was performed with statistical significance set at
p
< 0.05. IHC showed positive immunostaining with IL33 and IL35 in both OLP and NSI. Comparison of the numbers of IL33
+
and IL35
+
cells in OLP and NSI did not show any significant difference. In OLP, there were significantly more IL33
+
cells in the deeper connective tissue region than at the epithelial–connective tissue interface. Interestingly, all IL35
+
cells observed in both OLP and NSI tissues showed ovoid/plasmacytoid morphology. Double-labelling immunofluorescence showed that IL33 and IL35 expression was not localized within CD3
+
T-cells. The gene expression experiments showed significantly higher expression of EBI3 (fold regulation 14.02) in OLP when compared to the inflammatory controls. IL33 gene expression was not different between the groups. However, within the OLP tissues, there was a significantly higher expression of IL33 than EBI3. Our data demonstrate the expression of IL33 and IL35 in OLP lesions. Further studies are needed to understand the functional role of these cytokines in OLP pathogenesis.</description><identifier>ISSN: 0340-3696</identifier><identifier>EISSN: 1432-069X</identifier><identifier>DOI: 10.1007/s00403-018-1829-5</identifier><identifier>PMID: 29633015</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biopsy ; CD3 antigen ; Cytokines ; Dermatology ; Female ; Fluorescent Antibody Technique ; Gene expression ; Gene Expression Regulation ; Humans ; Immune response ; Immunofluorescence ; Immunohistochemistry ; Inflammation ; Inflammatory diseases ; Interleukin 1 ; Interleukin 12 ; Interleukin-33 - genetics ; Interleukin-33 - metabolism ; Interleukins - genetics ; Interleukins - metabolism ; Labeling ; Lichen planus ; Lichen Planus, Oral - immunology ; Lymphocytes T ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Mouth Mucosa - immunology ; Original Paper ; Paraffin ; Polymerase chain reaction ; RNA-directed DNA polymerase ; Skin diseases ; T-Lymphocytes, Regulatory - immunology</subject><ispartof>Archives of Dermatological Research, 2018-07, Vol.310 (5), p.431-441</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2018</rights><rights>Archives of Dermatological Research is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-832aeadf90dff9c2d602e66fe2c1917473f447cc52fe1ea83650471446695aeb3</citedby><cites>FETCH-LOGICAL-c372t-832aeadf90dff9c2d602e66fe2c1917473f447cc52fe1ea83650471446695aeb3</cites><orcidid>0000-0001-8096-4245</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00403-018-1829-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00403-018-1829-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29633015$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Javvadi, L. R.</creatorcontrib><creatorcontrib>Parachuru, V. P. B.</creatorcontrib><creatorcontrib>Milne, T. J.</creatorcontrib><creatorcontrib>Seymour, G. J.</creatorcontrib><creatorcontrib>Rich, Alison M.</creatorcontrib><title>Expression of IL33 and IL35 in oral lichen planus</title><title>Archives of Dermatological Research</title><addtitle>Arch Dermatol Res</addtitle><addtitle>Arch Dermatol Res</addtitle><description>Oral lichen planus (OLP) is a complex immunological disorder, mediated in part by the release of cytokines by activated T-cells. Recently, the role of novel cytokines including IL33 and IL35 has been described in various chronic inflammatory diseases. IL33, a member of the IL-1 superfamily of cytokines, functions as an ‘alarmin’ released after cell necrosis to alert the immune system to tissue damage or stress. IL35, a member of IL12 cytokine family, is produced by regulatory T-cells and suppresses the immune response. The expression of IL33 and IL35 is yet to be investigated in OLP. The aim of this study was to determine the presence and topographical distribution of IL33 and IL35 in OLP using immunohistochemistry and quantitative real-time reverse transcriptase polymerase chain reaction (qPCR). For IHC, formalin-fixed paraffin-embedded archival specimens of OLP (
n
= 10) and a non-specific inflammatory (NSI) control group (
n
= 9) were used. A double-labelling immunofluorescence technique was used to determine the expression of IL33 and IL35 on CD3
+
T-cells. In addition, 12 fresh tissue samples (OLP
n
= 6 and NSI controls
n
= 6) were used to determine the gene expression of IL33 and EBI3 (one chain of the dimeric IL35). Quantitative and qualitative analysis was performed with statistical significance set at
p
< 0.05. IHC showed positive immunostaining with IL33 and IL35 in both OLP and NSI. Comparison of the numbers of IL33
+
and IL35
+
cells in OLP and NSI did not show any significant difference. In OLP, there were significantly more IL33
+
cells in the deeper connective tissue region than at the epithelial–connective tissue interface. Interestingly, all IL35
+
cells observed in both OLP and NSI tissues showed ovoid/plasmacytoid morphology. Double-labelling immunofluorescence showed that IL33 and IL35 expression was not localized within CD3
+
T-cells. The gene expression experiments showed significantly higher expression of EBI3 (fold regulation 14.02) in OLP when compared to the inflammatory controls. IL33 gene expression was not different between the groups. However, within the OLP tissues, there was a significantly higher expression of IL33 than EBI3. Our data demonstrate the expression of IL33 and IL35 in OLP lesions. Further studies are needed to understand the functional role of these cytokines in OLP pathogenesis.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biopsy</subject><subject>CD3 antigen</subject><subject>Cytokines</subject><subject>Dermatology</subject><subject>Female</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Interleukin 1</subject><subject>Interleukin 12</subject><subject>Interleukin-33 - genetics</subject><subject>Interleukin-33 - metabolism</subject><subject>Interleukins - genetics</subject><subject>Interleukins - metabolism</subject><subject>Labeling</subject><subject>Lichen planus</subject><subject>Lichen Planus, Oral - immunology</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mouth Mucosa - immunology</subject><subject>Original Paper</subject><subject>Paraffin</subject><subject>Polymerase chain reaction</subject><subject>RNA-directed DNA polymerase</subject><subject>Skin diseases</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><issn>0340-3696</issn><issn>1432-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kE1LAzEQhoMottT-AC-y4MVLdPK9OUqpWih4UfAW0myiW7a7NemC_ntT1w8QzGVC5pk3w4PQKYFLAqCuEgAHhoGUmJRUY3GAxoQzikHqp0M0BsYBM6nlCE1TWkM-CjgFdYxGVEvGgIgxIvO3bfQp1V1bdKFYLBkrbFvtL6Ko81u0TdHU7sW3xbaxbZ9O0FGwTfLTrzpBjzfzh9kdXt7fLmbXS-yYojtcMmq9rYKGKgTtaCWBeimDp45oorhigXPlnKDBE29LJgVwRTiXUgvrV2yCLobcbexee592ZlMn55u8hO_6ZChQphiAIBk9_4Ouuz62ebtPikpKBM0UGSgXu5SiD2Yb642N74aA2Ss1g1KTlZq9UiPyzNlXcr_a-Opn4ltgBugApNxqn338_fr_1A8aa3zA</recordid><startdate>20180701</startdate><enddate>20180701</enddate><creator>Javvadi, L. R.</creator><creator>Parachuru, V. P. B.</creator><creator>Milne, T. J.</creator><creator>Seymour, G. J.</creator><creator>Rich, Alison M.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8096-4245</orcidid></search><sort><creationdate>20180701</creationdate><title>Expression of IL33 and IL35 in oral lichen planus</title><author>Javvadi, L. R. ; Parachuru, V. P. B. ; Milne, T. J. ; Seymour, G. J. ; Rich, Alison M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-832aeadf90dff9c2d602e66fe2c1917473f447cc52fe1ea83650471446695aeb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biopsy</topic><topic>CD3 antigen</topic><topic>Cytokines</topic><topic>Dermatology</topic><topic>Female</topic><topic>Fluorescent Antibody Technique</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunofluorescence</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Interleukin 1</topic><topic>Interleukin 12</topic><topic>Interleukin-33 - genetics</topic><topic>Interleukin-33 - metabolism</topic><topic>Interleukins - genetics</topic><topic>Interleukins - metabolism</topic><topic>Labeling</topic><topic>Lichen planus</topic><topic>Lichen Planus, Oral - immunology</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mouth Mucosa - immunology</topic><topic>Original Paper</topic><topic>Paraffin</topic><topic>Polymerase chain reaction</topic><topic>RNA-directed DNA polymerase</topic><topic>Skin diseases</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Javvadi, L. R.</creatorcontrib><creatorcontrib>Parachuru, V. P. B.</creatorcontrib><creatorcontrib>Milne, T. J.</creatorcontrib><creatorcontrib>Seymour, G. 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R.</au><au>Parachuru, V. P. B.</au><au>Milne, T. J.</au><au>Seymour, G. J.</au><au>Rich, Alison M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of IL33 and IL35 in oral lichen planus</atitle><jtitle>Archives of Dermatological Research</jtitle><stitle>Arch Dermatol Res</stitle><addtitle>Arch Dermatol Res</addtitle><date>2018-07-01</date><risdate>2018</risdate><volume>310</volume><issue>5</issue><spage>431</spage><epage>441</epage><pages>431-441</pages><issn>0340-3696</issn><eissn>1432-069X</eissn><abstract>Oral lichen planus (OLP) is a complex immunological disorder, mediated in part by the release of cytokines by activated T-cells. Recently, the role of novel cytokines including IL33 and IL35 has been described in various chronic inflammatory diseases. IL33, a member of the IL-1 superfamily of cytokines, functions as an ‘alarmin’ released after cell necrosis to alert the immune system to tissue damage or stress. IL35, a member of IL12 cytokine family, is produced by regulatory T-cells and suppresses the immune response. The expression of IL33 and IL35 is yet to be investigated in OLP. The aim of this study was to determine the presence and topographical distribution of IL33 and IL35 in OLP using immunohistochemistry and quantitative real-time reverse transcriptase polymerase chain reaction (qPCR). For IHC, formalin-fixed paraffin-embedded archival specimens of OLP (
n
= 10) and a non-specific inflammatory (NSI) control group (
n
= 9) were used. A double-labelling immunofluorescence technique was used to determine the expression of IL33 and IL35 on CD3
+
T-cells. In addition, 12 fresh tissue samples (OLP
n
= 6 and NSI controls
n
= 6) were used to determine the gene expression of IL33 and EBI3 (one chain of the dimeric IL35). Quantitative and qualitative analysis was performed with statistical significance set at
p
< 0.05. IHC showed positive immunostaining with IL33 and IL35 in both OLP and NSI. Comparison of the numbers of IL33
+
and IL35
+
cells in OLP and NSI did not show any significant difference. In OLP, there were significantly more IL33
+
cells in the deeper connective tissue region than at the epithelial–connective tissue interface. Interestingly, all IL35
+
cells observed in both OLP and NSI tissues showed ovoid/plasmacytoid morphology. Double-labelling immunofluorescence showed that IL33 and IL35 expression was not localized within CD3
+
T-cells. The gene expression experiments showed significantly higher expression of EBI3 (fold regulation 14.02) in OLP when compared to the inflammatory controls. IL33 gene expression was not different between the groups. However, within the OLP tissues, there was a significantly higher expression of IL33 than EBI3. Our data demonstrate the expression of IL33 and IL35 in OLP lesions. Further studies are needed to understand the functional role of these cytokines in OLP pathogenesis.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>29633015</pmid><doi>10.1007/s00403-018-1829-5</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-8096-4245</orcidid></addata></record> |
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| ispartof | Archives of Dermatological Research, 2018-07, Vol.310 (5), p.431-441 |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adult Aged Aged, 80 and over Biopsy CD3 antigen Cytokines Dermatology Female Fluorescent Antibody Technique Gene expression Gene Expression Regulation Humans Immune response Immunofluorescence Immunohistochemistry Inflammation Inflammatory diseases Interleukin 1 Interleukin 12 Interleukin-33 - genetics Interleukin-33 - metabolism Interleukins - genetics Interleukins - metabolism Labeling Lichen planus Lichen Planus, Oral - immunology Lymphocytes T Male Medicine Medicine & Public Health Middle Aged Mouth Mucosa - immunology Original Paper Paraffin Polymerase chain reaction RNA-directed DNA polymerase Skin diseases T-Lymphocytes, Regulatory - immunology |
| title | Expression of IL33 and IL35 in oral lichen planus |
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