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Review
. 2017 Mar 14:10:1561-1573.
doi: 10.2147/OTT.S126424. eCollection 2017.

Mechanism of immune evasion in breast cancer

Mozhi Wang  1 , Changwang Zhang  2 , Yongxi Song  2 , Zhenning Wang  2 , Yaojia Wang  1 , Fang Luo  1 , Yujie Xu  1 , Yi Zhao  1 , Zhonghua Wu  2 , Yingying Xu  1
Affiliations
Review

Mechanism of immune evasion in breast cancer

Mozhi Wang et al. Onco Targets Ther. .

Abstract

Breast cancer (BC) is the most common malignant tumor among women, with high morbidity and mortality. Its onset, development, metastasis, and prognosis vary among individuals due to the interactions between tumors and host immunity. Many diverse mechanisms have been associated with BC, with immune evasion being the most widely studied to date. Tumor cells can escape from the body's immune response, which targets abnormal components and foreign bodies, using different approaches including modification of surface antigens and modulation of the surrounding environment. In this review, we summarize the mechanisms and factors that impact the immunoediting process and analyze their functions in detail.

Keywords: PD-L1; apoptosis; breast cancer; cytokines; immune evasion; mechanism.

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Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
A summarized network of immune evasion mechanisms and their interactions. Abbreviations: IL, interleukin; TGF-β, transforming growth factor type beta; NK, natural killer; CTL, cytotoxic T lymphocyte; MHC, major histocompatibility complex; DC, dendritic cell; PD-1, programmed death receptor 1; PD-L1, PD-1 ligand; FasL, Fas ligand; Fas, factor-associated suicide; HLA, human leukocyte antigen; BC, breast cancer; Treg, regulatory T cell; CCL, C–C motif chemokine ligand; STAT, signal transducer and activator of transcription; NF-κB, nuclear factor-kappa B; TNF-α, tumor necrosis factor alpha.
Figure 2
Figure 2
Influences of Fas/FasL system on apoptosis. Note: This figure shows the way that Fas/FasL system applies to influence the apoptosis. In natural status, cells that can express Fas go through apoptosis after its combination to FasL in activated T cells. However, Fas is less expressed in BC cells and its specific intracellular signaling domain, the death domain (DD), is deficient. And the overexpression of FasL in activated T cells leads to T cells’ suicide. Abbreviations: FasL, Fas ligand; Fas, factor-associated suicide; DD, death domain; BC, breast cancer.
See this image and copyright information in PMC

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