Tumor-derived macrophage migration inhibitory factor (MIF) inhibits T lymphocyte activation

被引:51
作者
Yan, Xiaocai
Orentas, Rimas J.
Johnson, Bryon D.
机构
[1] Med Coll Wisconsin, Dept Pediat, Hematol Oncol Sect, MFRC 6011, Milwaukee, WI 53226 USA
[2] Childrens Hosp Wisconsin, Childrens Res Inst, Milwaukee, WI 53226 USA
关键词
migration inhibitory factor; tumor immunity; T cells; cytokines; cell activation;
D O I
10.1016/j.cyto.2006.01.006
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 a multi-functional cytokine that is considered a pro-inflammatory cytokine. However, our studies show that MIF, when produced in super-physiological levels by a murine neuroblastoma cell line (Neuro-2a) exceeding those normally seen during an immune response, inhibits cytokine-, CD3-, and allo-induced T-cell activation. MIF is also able to inhibit T cells that have already received an activation signal. The T-cell inhibitory effects of culture supernatants from neuroblastoma cells were reversed when the cells were transfected with dicer-gencrated si-RNA to MIF When T cells were activated in vitro by co-culture with interleukin (IL)-2 and IL-15 and analyzed for cytokine production in the presence or absence of MIF-containing culture supernatant, inhibition of T-cell proliferation and induced cell death were observed even as the treated T cells produced high levels of interfercm-gamma (IFN-gamma). The inhibitory effects of MIF were partially reversed when lymphocytes from IFN-gamma knockout mice were tested. We propose that the high levels of MIF produced by neuroblastoma cause activation induced T-cell death through an IFN-gamma pathway and may eliminate activated T cells from the tumor microenvironment and thus contribute to escape from immune surveillance. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:188 / 198
页数:11
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