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. 2012 Feb 23:3:21.
doi: 10.3389/fimmu.2012.00021. eCollection 2012.

Hypoxia promotes tumor growth in linking angiogenesis to immune escape

Affiliations

Hypoxia promotes tumor growth in linking angiogenesis to immune escape

Salem Chouaib et al. Front Immunol. .

"VSports注册入口" Abstract

Despite the impressive progress over the past decade, in the field of tumor immunology, such as the identification of tumor antigens and antigenic peptides, there are still many obstacles in eliciting an effective immune response to eradicate cancer. It has become increasingly clear that tumor microenvironment plays a crucial role in the control of immune protection. Tumors have evolved to utilize hypoxic stress to their own advantage by activating key biochemical and cellular pathways that are important in progression, survival, and metastasis. Hypoxia-inducible factor (HIF-1) and vascular endothelial growth factor (VEGF) play a determinant role in promoting tumor cell growth and survival. Hypoxia contributes to immune suppression by activating HIF-1 and VEGF pathways. Accumulating evidence suggests a link between hypoxia and tumor tolerance to immune surveillance through the recruitment of regulatory cells (regulatory T cells and myeloid derived suppressor cells). In this regard, hypoxia (HIF-1α and VEGF) is emerging as an attractive target for cancer therapy VSports手机版. How the microenvironmental hypoxia poses both obstacles and opportunities for new therapeutic immune interventions will be discussed. .

Keywords: HIFα; angiogenesis; hypoxia; immune tolerance; tumor progression V体育安卓版. .

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Figures

Figure 1
Figure 1
Role of hypoxia-induced VEGF in mediating immune tolerance. Diverse effects of hypoxia-induced VEGF on different components of the immune system (TAM, MDSC, DC, CTL, and T reg). In general, hypoxia-induced VEGF pool in tumor microenvironment (VEGF secreted by hypoxic tumor cells, TAM, MDSC, DC, and T reg) amplifies the activity of TAM, MDSC, and T reg while suppressing the function of CTL and delaying the maturation of DC cells. TAM, tumor-associated macrophages; MDSC, myeloid derived suppressor cells; DC, dendritic cells; CTL, cytotoxic T-lymphocyte; T reg, T regulatory cells.

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