Airway epithelial cell-derived insulin-like growth factor-1 triggers skewed CD8+ T cell polarization
Skewed CD8+ T cell responses are important in airway inflammation. This study investigates the role of the airway epithelial cell‐derived insulin‐like growth factor 1 (IGF1) in contributing to CD8+ T cell polarization. Expression of IGF1 in the airway epithelial cell line, RPMI2650 cells, was assess...
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Veröffentlicht in: | Cell biology international 2014-10, Vol.38 (10), p.1148-1154 |
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description | Skewed CD8+ T cell responses are important in airway inflammation. This study investigates the role of the airway epithelial cell‐derived insulin‐like growth factor 1 (IGF1) in contributing to CD8+ T cell polarization. Expression of IGF1 in the airway epithelial cell line, RPMI2650 cells, was assessed by quantitative real time RT‐PCR and Western blotting. The role of IGF1 in regulating CD8+ T cell activation was observed by coculture of mite allergen‐primed RPMI2650 cells and naïve CD8+ T cells. CD8+ T cell polarization was assessed by the carboxyfluorescein succinimidyl ester‐dilution assay and the determination of cytotoxic cytokine levels in the culture medium. Exposure to mite allergen, Der p1, increased the expression of IGF1 by RPMI2650 cells. The epithelial cell‐derived IGF1 prevented the activation‐induced cell death by inducing the p53 gene hypermethylation. Mite allergen‐primed RPMI2650 cells induced an antigen‐specific CD8+ T cell polarization. We conclude that mite allergens induce airway epithelial cell line, RPMI2650 cells, to produce IGF1; the latter contributes to antigen‐specific CD8+ T cell polarization. |
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This study investigates the role of the airway epithelial cell‐derived insulin‐like growth factor 1 (IGF1) in contributing to CD8+ T cell polarization. Expression of IGF1 in the airway epithelial cell line, RPMI2650 cells, was assessed by quantitative real time RT‐PCR and Western blotting. The role of IGF1 in regulating CD8+ T cell activation was observed by coculture of mite allergen‐primed RPMI2650 cells and naïve CD8+ T cells. CD8+ T cell polarization was assessed by the carboxyfluorescein succinimidyl ester‐dilution assay and the determination of cytotoxic cytokine levels in the culture medium. Exposure to mite allergen, Der p1, increased the expression of IGF1 by RPMI2650 cells. The epithelial cell‐derived IGF1 prevented the activation‐induced cell death by inducing the p53 gene hypermethylation. Mite allergen‐primed RPMI2650 cells induced an antigen‐specific CD8+ T cell polarization. We conclude that mite allergens induce airway epithelial cell line, RPMI2650 cells, to produce IGF1; the latter contributes to antigen‐specific CD8+ T cell polarization.</description><identifier>ISSN: 1065-6995</identifier><identifier>EISSN: 1095-8355</identifier><identifier>DOI: 10.1002/cbin.10313</identifier><identifier>PMID: 24844927</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>airway ; Antigens, Dermatophagoides - pharmacology ; Arthropod Proteins - pharmacology ; CD8 T cells ; CD8-Positive T-Lymphocytes - cytology ; CD8-Positive T-Lymphocytes - drug effects ; CD8-Positive T-Lymphocytes - immunology ; Cell Line ; Cell Proliferation - drug effects ; Cell Shape - drug effects ; Cysteine Endopeptidases - pharmacology ; DNA Methylation - drug effects ; epithelial cells ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Humans ; Insulin-Like Growth Factor I - isolation & purification ; Insulin-Like Growth Factor I - metabolism ; Insulin-Like Growth Factor I - pharmacology ; insulin-like growth factor-1 ; MAP Kinase Kinase Kinases - metabolism ; P53 gene methylation ; Signal Transduction - drug effects ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Up-Regulation - drug effects</subject><ispartof>Cell biology international, 2014-10, Vol.38 (10), p.1148-1154</ispartof><rights>2014 International Federation for Cell Biology</rights><rights>2014 International Federation for Cell Biology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4283-483623fe79252858c5f4125cfabc4038a49dc0e27f9229a25f850f95b7b32f053</citedby><cites>FETCH-LOGICAL-c4283-483623fe79252858c5f4125cfabc4038a49dc0e27f9229a25f850f95b7b32f053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcbin.10313$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcbin.10313$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24844927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zou, Jian-Yong</creatorcontrib><creatorcontrib>Huang, Shao-hong</creatorcontrib><creatorcontrib>Li, Yun</creatorcontrib><creatorcontrib>Chen, Hui-guo</creatorcontrib><creatorcontrib>Rong, Jian</creatorcontrib><creatorcontrib>Ye, Sheng</creatorcontrib><title>Airway epithelial cell-derived insulin-like growth factor-1 triggers skewed CD8+ T cell polarization</title><title>Cell biology international</title><addtitle>Cell Biol Int</addtitle><description>Skewed CD8+ T cell responses are important in airway inflammation. This study investigates the role of the airway epithelial cell‐derived insulin‐like growth factor 1 (IGF1) in contributing to CD8+ T cell polarization. Expression of IGF1 in the airway epithelial cell line, RPMI2650 cells, was assessed by quantitative real time RT‐PCR and Western blotting. The role of IGF1 in regulating CD8+ T cell activation was observed by coculture of mite allergen‐primed RPMI2650 cells and naïve CD8+ T cells. CD8+ T cell polarization was assessed by the carboxyfluorescein succinimidyl ester‐dilution assay and the determination of cytotoxic cytokine levels in the culture medium. Exposure to mite allergen, Der p1, increased the expression of IGF1 by RPMI2650 cells. The epithelial cell‐derived IGF1 prevented the activation‐induced cell death by inducing the p53 gene hypermethylation. Mite allergen‐primed RPMI2650 cells induced an antigen‐specific CD8+ T cell polarization. We conclude that mite allergens induce airway epithelial cell line, RPMI2650 cells, to produce IGF1; the latter contributes to antigen‐specific CD8+ T cell polarization.</description><subject>airway</subject><subject>Antigens, Dermatophagoides - pharmacology</subject><subject>Arthropod Proteins - pharmacology</subject><subject>CD8 T cells</subject><subject>CD8-Positive T-Lymphocytes - cytology</subject><subject>CD8-Positive T-Lymphocytes - drug effects</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>Cell Line</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Shape - drug effects</subject><subject>Cysteine Endopeptidases - pharmacology</subject><subject>DNA Methylation - drug effects</subject><subject>epithelial cells</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Humans</subject><subject>Insulin-Like Growth Factor I - isolation & purification</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>insulin-like growth factor-1</subject><subject>MAP Kinase Kinase Kinases - metabolism</subject><subject>P53 gene methylation</subject><subject>Signal Transduction - drug effects</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Up-Regulation - drug effects</subject><issn>1065-6995</issn><issn>1095-8355</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1uEzEURi0Eom1gwwMgS2wQlYt_x_ayDTRUtEVCRbCzPB47dePMBHumIX16Jk3bBQtW9y7Od-7VB8Abgo8IxvSjq2M7boywZ2CfYC2QYkI83-6VQJXWYg8clHKDMSFcVS_BHuWKc03lPmiOY17bDfSr2F_7FG2CzqeEGp_jrW9gbMuQYotSXHg4z926v4bBur7LiMA-x_nc5wLLwq9HePpJHcKrewFcdcnmeGf72LWvwItgU_GvH-YE_Dj9fDX9gs6_zc6mx-fIcaoY4opVlAUvNRVUCeVE4IQKF2ztOGbKct047KkMmlJtqQhK4KBFLWtGAxZsAt7vvKvc_R586c0ylu03tvXdUAypSMWlluOhCXj3D3rTDbkdvxspXklJJeEj9WFHudyVkn0wqxyXNm8MwWbbvdl2b-67H-G3D8qhXvrmCX0sewTIDljH5Df_UZnpydnloxTtMrH0_s9TxuaFqSSTwvy8nJkLzn7x2fdT85X9BTPWnCY</recordid><startdate>201410</startdate><enddate>201410</enddate><creator>Zou, Jian-Yong</creator><creator>Huang, Shao-hong</creator><creator>Li, Yun</creator><creator>Chen, Hui-guo</creator><creator>Rong, Jian</creator><creator>Ye, Sheng</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201410</creationdate><title>Airway epithelial cell-derived insulin-like growth factor-1 triggers skewed CD8+ T cell polarization</title><author>Zou, Jian-Yong ; Huang, Shao-hong ; Li, Yun ; Chen, Hui-guo ; Rong, Jian ; Ye, Sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4283-483623fe79252858c5f4125cfabc4038a49dc0e27f9229a25f850f95b7b32f053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>airway</topic><topic>Antigens, Dermatophagoides - pharmacology</topic><topic>Arthropod Proteins - pharmacology</topic><topic>CD8 T cells</topic><topic>CD8-Positive T-Lymphocytes - cytology</topic><topic>CD8-Positive T-Lymphocytes - drug effects</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>Cell Line</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Shape - drug effects</topic><topic>Cysteine Endopeptidases - pharmacology</topic><topic>DNA Methylation - drug effects</topic><topic>epithelial cells</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Humans</topic><topic>Insulin-Like Growth Factor I - isolation & purification</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Insulin-Like Growth Factor I - pharmacology</topic><topic>insulin-like growth factor-1</topic><topic>MAP Kinase Kinase Kinases - metabolism</topic><topic>P53 gene methylation</topic><topic>Signal Transduction - drug effects</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zou, Jian-Yong</creatorcontrib><creatorcontrib>Huang, Shao-hong</creatorcontrib><creatorcontrib>Li, Yun</creatorcontrib><creatorcontrib>Chen, Hui-guo</creatorcontrib><creatorcontrib>Rong, Jian</creatorcontrib><creatorcontrib>Ye, Sheng</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zou, Jian-Yong</au><au>Huang, Shao-hong</au><au>Li, Yun</au><au>Chen, Hui-guo</au><au>Rong, Jian</au><au>Ye, Sheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Airway epithelial cell-derived insulin-like growth factor-1 triggers skewed CD8+ T cell polarization</atitle><jtitle>Cell biology international</jtitle><addtitle>Cell Biol Int</addtitle><date>2014-10</date><risdate>2014</risdate><volume>38</volume><issue>10</issue><spage>1148</spage><epage>1154</epage><pages>1148-1154</pages><issn>1065-6995</issn><eissn>1095-8355</eissn><abstract>Skewed CD8+ T cell responses are important in airway inflammation. This study investigates the role of the airway epithelial cell‐derived insulin‐like growth factor 1 (IGF1) in contributing to CD8+ T cell polarization. Expression of IGF1 in the airway epithelial cell line, RPMI2650 cells, was assessed by quantitative real time RT‐PCR and Western blotting. The role of IGF1 in regulating CD8+ T cell activation was observed by coculture of mite allergen‐primed RPMI2650 cells and naïve CD8+ T cells. CD8+ T cell polarization was assessed by the carboxyfluorescein succinimidyl ester‐dilution assay and the determination of cytotoxic cytokine levels in the culture medium. Exposure to mite allergen, Der p1, increased the expression of IGF1 by RPMI2650 cells. The epithelial cell‐derived IGF1 prevented the activation‐induced cell death by inducing the p53 gene hypermethylation. Mite allergen‐primed RPMI2650 cells induced an antigen‐specific CD8+ T cell polarization. We conclude that mite allergens induce airway epithelial cell line, RPMI2650 cells, to produce IGF1; the latter contributes to antigen‐specific CD8+ T cell polarization.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24844927</pmid><doi>10.1002/cbin.10313</doi><tpages>7</tpages></addata></record> |
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subjects | airway Antigens, Dermatophagoides - pharmacology Arthropod Proteins - pharmacology CD8 T cells CD8-Positive T-Lymphocytes - cytology CD8-Positive T-Lymphocytes - drug effects CD8-Positive T-Lymphocytes - immunology Cell Line Cell Proliferation - drug effects Cell Shape - drug effects Cysteine Endopeptidases - pharmacology DNA Methylation - drug effects epithelial cells Epithelial Cells - cytology Epithelial Cells - drug effects Epithelial Cells - metabolism Extracellular Signal-Regulated MAP Kinases - metabolism Humans Insulin-Like Growth Factor I - isolation & purification Insulin-Like Growth Factor I - metabolism Insulin-Like Growth Factor I - pharmacology insulin-like growth factor-1 MAP Kinase Kinase Kinases - metabolism P53 gene methylation Signal Transduction - drug effects Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Up-Regulation - drug effects |
title | Airway epithelial cell-derived insulin-like growth factor-1 triggers skewed CD8+ T cell polarization |
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