Tumor-infiltrating, myeloid-derived suppressor cells inhibit T cell activity by nitric oxide production in an intracranial rat glioma plus vaccination model

被引：69

作者：

Jia, Wentao ^{[1
,2
]}

Jackson-Cook, Colleen ^{[3
]}

Graf, Martin R. ^{[1
,2
]}

机构：

[1] Virginia Commonwealth Univ, Harold F Young Neurosurg Ctr, Dept Neurosurg, Richmond, VA 23298 USA

[2] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA 23298 USA

[3] Virginia Commonwealth Univ, Med Ctr, Dept Pathol, Richmond, VA 23298 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2010年 / 223卷 / 1-2期

基金：

美国国家卫生研究院;

关键词：

Brain tumor-associated immunosuppression; Malignant glioma; Myeloid-derived suppressor cells; Nitric oxide; CENTRAL-NERVOUS-SYSTEM; DENDRITIC CELLS; MALIGNANT GLIOMA; TOLERANCE; IMMUNOSUPPRESSION; SURVIVAL; DYSFUNCTION; ACTIVATION; MECHANISMS; MEDIATION;

D O I：

10.1016/j.jneuroim.2010.03.011

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

In rats bearing an intracranial T9 glioma, immunization with tumor antigens induces myeloid suppressor cells, which express neutrophil (His48) and monocyte (CD11bc) markers, to infiltrate the tumors. The His48(+)/CD11bc(+) cells were not derived from CNS microglia but were hematogenous; suppressed multiple T cell effector functions; and are myeloid-derived suppressor cells (MDSC). The glioma-infiltrating MDSC expressed arginase I, iNOS, indoleamine 2,3-dioxygenase and TGF-beta; however, inhibitor/blocking studies demonstrated that NO production was the primary mechanism of suppression which induced T cell apoptosis. These findings suggest that neuro-immunomodulation by MDSC in rat gliomas maybe mediated by a pathway requiring NO production. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：20 / 30

页数：11

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