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Airway epithelial cell‐derived insulin‐like growth factor‐1 triggers skewed CD8 + T cell polarization
Author(s) -
Zou JianYong,
Huang Shaohong,
Li Yun,
Chen Huiguo,
Rong Jian,
Ye Sheng
Publication year - 2014
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10313
Subject(s) - cytotoxic t cell , cd8 , t cell , biology , cell , cell culture , cell growth , cytokine , microbiology and biotechnology , immunology , antigen , chemistry , immune system , in vitro , biochemistry , genetics
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.