Elevated CD3+ and CD8+ tumor-infiltrating immune cells correlate with prolonged survival in glioblastoma patients despite integrated immunosuppressive mechanisms in the tumor microenvironment and at the systemic level

被引：318

作者：

Kmiecik, Justyna ^{[1
]}

Poli, Aurelie ^{[1
]}

Brons, Nicolaas H. C.

Waha, Andreas ^{[2
]}

Eide, Geir Egil ^{[3
,4
]}

Enger, Per Oyvind ^{[5
]}

Zimmer, Jacques

Chekenya, Martha ^{[1
,6
]}

机构：

[1] Univ Bergen, Dept Biomed, N-5009 Bergen, Norway

[2] Univ Hosp, Dept Neuropathol, Bonn, Germany

[3] Haukeland Hosp, Clin Res Ctr, N-5021 Bergen, Norway

[4] Univ Bergen, Dept Global Publ Hlth & Primary Care, N-5020 Bergen, Norway

[5] Haukeland Hosp, Dept Neurosurg, N-5021 Bergen, Norway

[6] Univ Bergen, Dept Clin Dent, N-5009 Bergen, Norway

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2013年 / 264卷 / 1-2期

关键词：

GBM; Tumor infiltrating cells; Regulatory T cells; Antigen presenting cells; REGULATORY T-CELLS; MGMT PROMOTER METHYLATION; NATURAL-KILLER-CELLS; NK CELLS; ADJUVANT TEMOZOLOMIDE; PROGNOSTIC VALUE; RECEPTOR; CANCER; EXPRESSION; NKG2D;

D O I：

10.1016/j.jneuroim.2013.08.013

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

We characterized GBM patients' tumor and systemic immune contexture with aim to reveal the mechanisms of immunological escape, their impact on patient outcome, and identify targets for immunotherapy. Increased CD3 T-cell infiltration was associated with prolonged survival independent of age, MGMT promoter methylation and post-operative treatment that implies potential for immunotherapy for GBM. Several mechanisms of escape were identified: within the tumor microenvironment: induced cD8+cD28 Foxp3 Tre that may tolerize antigen presenting cells, elevated CD73 and CD39 ectonucleotidases that suppress T-cell function, and at the systemic level: elevated IL-10 levels in serum, diminished helper T-cell counts, and upregulated inhibitory CTLA-4. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.

引用

页码：71 / 83

页数：13

共 64 条

[1] Determinants of human B cell migration across brain endothelial cells [J].