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
Hauptverfasser: Zou, Jian-Yong, Huang, Shao-hong, Li, Yun, Chen, Hui-guo, Rong, Jian, Ye, Sheng
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creator Zou, Jian-Yong
Huang, Shao-hong
Li, Yun
Chen, Hui-guo
Rong, Jian
Ye, Sheng
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.
doi_str_mv 10.1002/cbin.10313
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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. 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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 ; 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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 &amp; 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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.</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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