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Tumor inhibition or tumor promotion? The duplicity of CXCR3 in cancer.
Journal of Leukocyte Biology ( IF 3.6 ) Pub Date : 2020-08-03 , DOI: 10.1002/jlb.5mr0320-205r
Eleonora Russo 1 , Angela Santoni 1, 2 , Giovanni Bernardini 1
Journal of Leukocyte Biology ( IF 3.6 ) Pub Date : 2020-08-03 , DOI: 10.1002/jlb.5mr0320-205r
Eleonora Russo 1 , Angela Santoni 1, 2 , Giovanni Bernardini 1
Affiliation
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Tumor tissue includes cancer cells and normal stromal cells such as vascular endothelial cells, connective tissue cells (cancer associated fibroblast, mesenchymal stem cell), and immune cells (tumor‐infiltrating lymphocytes or TIL, dendritic cells, eosinophils, basophils, mast cells, tumor‐associated macrophages or TAM, myeloid‐derived suppressor cells or MDSC). Anti‐tumor activity is mainly mediated by infiltration of NK cells, Th1 and CD8+ T cells, and correlates with expression of NK cell and T cell attracting chemokines. Nevertheless, cancer cells hijack tissue homeostasis through secretion of cytokines and chemokines that mediate not only the induction of an inflamed status that supports cancer cell survival and growth, but also the recruitment and/or activation of immune suppressive cells. CXCL9, CXCL10, and CXCL11 are known for their tumor‐inhibiting properties, but their overexpression in several hematologic and solid tumors correlates with disease severity, suggesting a role in tumor promotion. The dichotomous nature of CXCR3 ligands activity mainly depends on several molecular mechanisms induced by cancer cells themselves able to divert immune responses and to alter the whole local environment. A deep understanding of the nature of such phenomenon may provide a rationale to build up a CXCR3/ligand axis targeting strategy. In this review, we will discuss the role of CXCR3 in cancer progression and in regulation of anti‐tumor immune response and immunotherapy.
中文翻译：
抑癌还是促进肿瘤？CXCR3在癌症中的双重性。
肿瘤组织包括癌细胞和正常基质细胞，例如血管内皮细胞，结缔组织细胞（与癌相关的成纤维细胞，间充质干细胞）和免疫细胞（肿瘤浸润淋巴细胞或TIL，树突状细胞，嗜酸性粒细胞，嗜碱性粒细胞，肥大细胞，肿瘤）巨噬细胞或TAM，髓样抑制细胞或MDSC）。抗肿瘤活性主要由NK细胞，Th1和CD8 +的浸润介导T细胞，并与NK细胞和T细胞吸引趋化因子的表达相关。然而，癌细胞通过细胞因子和趋化因子的分泌劫持了组织的动态平衡，所述细胞因子和趋化因子不仅介导了支持癌细胞存活和生长的发炎状态的诱导，而且还介导了免疫抑制细胞的募集和/或激活。CXCL9，CXCL10和CXCL11具有抑制肿瘤的特性，但在一些血液学和实体瘤中的过表达与疾病的严重程度有关，提示其在肿瘤促进中的作用。CXCR3配体活性的二分性主要取决于癌细胞自身诱导的几种分子机制，这些分子机制能够转移免疫反应并改变整个局部环境。对这种现象的性质的深入了解可能为建立CXCR3 /配体轴靶向策略提供依据。在这篇综述中，我们将讨论CXCR3在癌症进展以及抗肿瘤免疫应答和免疫疗法调节中的作用。
更新日期：2020-08-04
中文翻译：
抑癌还是促进肿瘤？CXCR3在癌症中的双重性。
肿瘤组织包括癌细胞和正常基质细胞，例如血管内皮细胞，结缔组织细胞（与癌相关的成纤维细胞，间充质干细胞）和免疫细胞（肿瘤浸润淋巴细胞或TIL，树突状细胞，嗜酸性粒细胞，嗜碱性粒细胞，肥大细胞，肿瘤）巨噬细胞或TAM，髓样抑制细胞或MDSC）。抗肿瘤活性主要由NK细胞，Th1和CD8 +的浸润介导T细胞，并与NK细胞和T细胞吸引趋化因子的表达相关。然而，癌细胞通过细胞因子和趋化因子的分泌劫持了组织的动态平衡，所述细胞因子和趋化因子不仅介导了支持癌细胞存活和生长的发炎状态的诱导，而且还介导了免疫抑制细胞的募集和/或激活。CXCL9，CXCL10和CXCL11具有抑制肿瘤的特性，但在一些血液学和实体瘤中的过表达与疾病的严重程度有关，提示其在肿瘤促进中的作用。CXCR3配体活性的二分性主要取决于癌细胞自身诱导的几种分子机制，这些分子机制能够转移免疫反应并改变整个局部环境。对这种现象的性质的深入了解可能为建立CXCR3 /配体轴靶向策略提供依据。在这篇综述中，我们将讨论CXCR3在癌症进展以及抗肿瘤免疫应答和免疫疗法调节中的作用。
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