Glucocorticoid-induced MIF expression by human CEM T cells

被引:36
作者
Leng, Lin [1 ]
Wang, Wenkui [4 ]
Roger, Thierry [2 ,3 ]
Merk, Melanie [1 ]
Wuttke, Martina [5 ]
Calandra, Thierry [2 ,3 ]
Bucala, Richard [1 ]
机构
[1] Yale Univ, Sch Med, New Haven, CT 06520 USA
[2] CHU Vaudois, Dept Med, Infect Dis Serv, Lausanne, Switzerland
[3] Univ Lausanne, Lausanne, Switzerland
[4] Shanxi Agr Univ, Taigu, Peoples R China
[5] Bayer Crop Sci AG, Monheim, Germany
基金
瑞士国家科学基金会;
关键词
Glucocorticoid receptor; Inflammation; T cell; Promoter; MIGRATION-INHIBITORY FACTOR; INNATE IMMUNE-RESPONSES; REGULATORY ROLE; RHEUMATOID-ARTHRITIS; MACROPHAGE; GENE; CYTOKINE; KINASE; ACTIVATION; PHOSPHATASE-1;
D O I
10.1016/j.cyto.2009.07.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Macrophage migration inhibitory factor (MIF) is an upstream activator of the immune response that counter-regulates the immunosuppressive effects of glucocorticoids. While MIF is released by cells in response to diverse microbial and invasive stimuli, evidence that glucocorticoids in low concentrations also induce MIF secretion suggests an additional regulatory relationship between these mediators. We investigated the expression of MIF from the human CEM T cell line, which exists in two well-characterized, glucocorticoid-sensitive (CEM-C7) and glucocorticoid-resistant (CEM-C1) variant clones. Dexamethasone in low concentrations induced MIF secretion from CEM-C7 but not CEM-C1 T cells by a bell-shaped dose response that was similar to that reported previously for the release of MIF by monocytes/macrophages. Glucocorticoid stimulation of CEM-C7 T cells was accompanied by an MIF transcriptional response, which by promoter analysis was found to involve the GRE and ATF/CRE transcription factor binding sites. These data support a glucocorticoid-mediated MIF secretion response by T cells that may contribute to the regulation of the adaptive immune response. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:177 / 185
页数:9
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