Myeloid suppressor cells in cancer and autoimmunity

被引:137
作者
Sica, Antonio [1 ,2 ,4 ]
Massarotti, Marco [2 ,3 ]
机构
[1] Univ Piemonte Orientale Amedeo Avogadro, Dept Pharmaceut Sci, Via Bovio 6, Novara, Italy
[2] Humanitas Clin & Res Ctr, Via Manzoni 56, I-20089 Milan, Italy
[3] Univ Hosp Morecambe Bay NHS Fdn Trust, Dept Rheumatol, Royal Lancaster Infirm, Ashton Rd, Lancaster LA1 4RP, England
[4] Ctr Translat Res Autoimmune & Allerg Dis, CAAD, Novara, Italy
关键词
TUMOR-ASSOCIATED MACROPHAGES; DENDRITIC CELLS; GUT MICROBIOTA; T-CELL; METABOLITE BUTYRATE; C/EBP-BETA; TH17; CELLS; POLARIZATION; INDUCTION; DISEASE;
D O I
10.1016/j.jaut.2017.07.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
A bottleneck for immunotherapy of cancer is the immunosuppressive microenvironment in which the tumor cells proliferate. Cancers harness the immune regulatory mechanism that prevents autoimmunity from evading immunosurveillance and promoting immune destruction. Regulatory T cells, myeloid suppressor cells, inhibitory cytokines and immune checkpoint receptors are the major components of the immune system acting in concert with cancer cells and causing the subversion of anti-tumor immunity. This redundant immunosuppressive network poses an impediment to efficacious immunotherapy by facilitating tumor progression. Tumor-associated myeloid cells comprise heterogeneous populations acting systemically (myeloid-derived suppressor cells/MDSCs) and/or locally in the tumor microenvironment (MDSCs and tumor-associated macrophages/TAMs). Both populations promote cancer cell proliferation and survival, angiogenesis and lymphangiogenesis and elicit immunosuppression through different pathways, including the expression of immunosuppressive cytokines and checkpoint inhibitors. Several evidences have demonstrated that myeloid cells can express different functional programs in response to different microenvironmental signals, a property defined as functional plasticity. The opposed extremes of this functional flexibility are generally represented by the classical macrophage activation, which identifies inflammatory and cytotoxic M1 polarized macrophages, and the alternative state of macrophage activation, which identifies M2 polarized anti-inflammatory and immunosuppressive macrophages. Functional skewing of myeloid cells occurs in vivo under physiological and pathological conditions, including cancer and autoimmunity. Here we discuss how myeloid suppressor cells can on one hand support tumor growth and, on the other, limit autoimmune respones, indicating that their therapeutic reprogramming can generate opportunities in relieving immunosuppression in the tumor microenvironment or reinstating tolerance in autoimmune conditions. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:117 / 125
页数:9
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