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由CD8 + T细胞介导的EBI-3缺陷小鼠肺黑色素瘤转移的免疫监视。

Immunosurveillance of lung melanoma metastasis in EBI-3-deficient mice mediated by CD8+ T cells.

作者信息

Sauer Kerstin A, Maxeiner Joachim H, Karwot Roman, Scholtes Petra, Lehr Hans A, Birkenbach Mark, Blumberg Richard S, Finotto Susetta

机构信息

Laboratory of Cellular and Molecular Immunology of the Lung, I. Medical Clinic, University of Mainz, Germany.

出版信息

J Immunol. 2008 Nov 1;181(9):6148-57. doi: 10.4049/jimmunol.181.9.6148.

DOI:10.4049/jimmunol.181.9.6148
PMID:18941205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3996841/
Abstract

EBV-induced gene 3 (EBI-3) codes for a soluble type I receptor homologous to the p40 subunit of IL-12 that is expressed by APCs following activation. In this study, we assessed the role of EBI-3 in a model of lung melanoma metastasis. Intravenous injection of the B16-F10 cell line resulted in a significant reduction of lung tumor metastasis in EBI-3(-/-) recipient mice compared with wild-type mice. The immunological finding accompanying this effect was the expansion of a newly described cell subset called IFN-gamma producing killer dendritic cells associated with CD8(+) T cell responses in the lung of EBI-3(-/-) mice including IFN-gamma release and TNF-alpha-induced programmed tumor cell death. Depletion of CD8(+) T cells as well as targeting T-bet abrogated the protective effects of EBI-3 deficiency on lung melanoma metastases. Finally, adoptive transfer of EBI-3(-/-) CD8(+) T cells into tumor bearing wild-type mice inhibited lung metastasis in recipient mice. Taken together, these data demonstrate that targeting EBI-3 leads to a T-bet-mediated antitumor CD8(+) T cell responses in the lung.

摘要

EB病毒诱导基因3（EBI-3）编码一种可溶性I型受体，与白细胞介素12的p40亚基同源，在激活后由抗原呈递细胞（APC）表达。在本研究中，我们评估了EBI-3在肺黑色素瘤转移模型中的作用。与野生型小鼠相比，静脉注射B16-F10细胞系导致EBI-3基因敲除（EBI-3(-/-)）受体小鼠的肺肿瘤转移显著减少。伴随这种效应的免疫学发现是一种新描述的细胞亚群的扩增，即产生γ干扰素的杀伤性树突状细胞，其与EBI-3(-/-)小鼠肺中的CD8(+) T细胞反应相关，包括γ干扰素释放和肿瘤坏死因子α诱导的程序性肿瘤细胞死亡。去除CD8(+) T细胞以及靶向T-bet消除了EBI-3缺陷对肺黑色素瘤转移的保护作用。最后，将EBI-3(-/-) CD8(+) T细胞过继转移到荷瘤野生型小鼠中可抑制受体小鼠的肺转移。综上所述，这些数据表明靶向EBI-3可导致肺中T-bet介导的抗肿瘤CD8(+) T细胞反应。

相似文献

[1]
Immunosurveillance of lung melanoma metastasis in EBI-3-deficient mice mediated by CD8+ T cells.

J Immunol. 2008-11-1

[2]
Lung CD11c+ cells from mice deficient in Epstein-Barr virus-induced gene 3 (EBI-3) prevent airway hyper-responsiveness in experimental asthma.

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[3]
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[4]
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J Immunol. 2004-2-1

[5]
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J Immunol. 2001-6-15

[6]
Type 1 and type 2 CD8+ effector T cell subpopulations promote long-term tumor immunity and protection to progressively growing tumor.

J Immunol. 2000-1-15

[7]
NK and CD8+ T cell-mediated eradication of poorly immunogenic B16-F10 melanoma by the combined action of IL-12 gene therapy and 4-1BB costimulation.

Int J Cancer. 2004-4-20

[8]
Differential requirement of perforin and IFN-gamma in CD8 T cell-mediated immune responses against B16.F10 melanoma cells expressing a viral antigen.

Eur J Immunol. 2000-9

[9]
Interleukin-33 pretreatment promotes metastatic growth of murine melanoma by reducing the cytotoxic capacity of CD8 T cells and enhancing regulatory T cells.

Cancer Immunol Immunother. 2020-4-13

[10]
Adoptive transfer of Tc1 or Tc17 cells elicits antitumor immunity against established melanoma through distinct mechanisms.

J Immunol. 2013-1-11

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[3]
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[4]
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J Clin Invest. 2020-11-2

[5]
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[6]
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[7]
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Immunity. 2019-4-16

[8]
IL-27 confers a protumorigenic activity of regulatory T cells via CD39.

Proc Natl Acad Sci U S A. 2019-2-4

[9]
Epstein-Barr Virus-Induced Gene 3 (EBI3) Blocking Leads to Induce Antitumor Cytotoxic T Lymphocyte Response and Suppress Tumor Growth in Colorectal Cancer by Bidirectional Reciprocal-Regulation STAT3 Signaling Pathway.

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[10]
Epstein-Barr virus-induced gene 3-deficiency leads to impaired antitumor T-cell responses and accelerated tumor growth.

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本文引用的文献

[1]
T-bet plays a key role in NK-mediated control of melanoma metastatic disease.

J Immunol. 2008-6-15

[2]
Protective role of nuclear factor of activated T cells 2 in CD8+ long-lived memory T cells in an allergy model.

J Allergy Clin Immunol. 2008-4

[3]
The inhibitory cytokine IL-35 contributes to regulatory T-cell function.

Nature. 2007-11-22

[4]
Putative IKDCs are functionally and developmentally similar to natural killer cells, but not to dendritic cells.

J Exp Med. 2007-10-29

[5]
Development and function of murine B220+CD11c+NK1.1+ cells identify them as a subset of NK cells.

J Exp Med. 2007-10-29

[6]
Lung CD11c+ cells from mice deficient in Epstein-Barr virus-induced gene 3 (EBI-3) prevent airway hyper-responsiveness in experimental asthma.

Eur J Immunol. 2007-6

[7]
Isolation of CD4+ T cells from murine lungs: a method to analyze ongoing immune responses in the lung.

Nat Protoc. 2006

[8]
A method to enable the investigation of murine bronchial immune cells, their cytokines and mediators.

Nat Protoc. 2007

[9]
Melanoma biology and new targeted therapy.

Nature. 2007-2-22

[10]
Therapy-induced tumor immunosurveillance involves IFN-producing killer dendritic cells.

Cancer Res. 2007-2-1

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