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The spleen contributes to the increase in PMN-MDSCs in orthotopic H22 hepatoma mice.
Molecular Immunology ( IF 3.2 ) Pub Date : 2020-07-10 , DOI: 10.1016/j.molimm.2020.07.002
Bao-Hua Li 1 , Wei Jiang 2 , Shu Zhang 3 , Na Huang 1 , Jin Sun 2 , Jun Yang 4 , Zong-Fang Li 2
Affiliation  

Myeloid-derived suppressor cells (MDSCs) are classified into polymorphonuclear (PMN)-MDSCs and monocytic (M)-MDSCs. The predominant subtype of MDSCs in hepatocellular carcinoma (HCC) is still elusive. The spleen is the largest immune organ in the body and is the origin of many cells. It is still unknown whether the spleen is the origin of MDSCs. In this study, we investigated the expression, origin and mobilization of the predominant MDSC subtype in H22 orthotopic hepatoma mice. Compared with M-MDSCs, PMN-MDSCs were increased and dominant in the spleen, peripheral blood and tumor tissues. Splenectomy could decrease the percentages of PMN-MDSCs in the peripheral blood and tumor tissues, increase the frequencies of NK cells in the peripheral blood and CD3+CD4+T, CD3+CD8+T, NK and NKT cells in the tumor tissues, reduce the tumor weight and the amounts of ascites, and prolong survival time in hepatoma mice. The levels of chemokine (CC motif) ligand 9 (CCL9) and chemokine (CC motif) ligand 2 (CCL2) were elevated in the peripheral blood of tumor-bearing (TB) mice, and their receptors CCR1 and CCR2 were expressed on spleen PMN-MDSCs. Migration assay showed that CCL2 and CCL9 could attract spleen PMN-MDSCs in vitro. These results indicate that PMN-MDSCs were increased and dominant in orthotopic H22 hepatoma mice, the spleen contributed to the increase of PMN-MDSCs, and PMN-MDSCs could be mobilized from the spleen to the peripheral blood by CCL9 and CCL2, thus facilitated tumor growth.



中文翻译:

脾脏有助于原位H22肝癌小鼠PMN-MDSCs的增加。

骨髓来源的抑制细胞(MDSC)分为多形核(PMN)-MDSC和单核细胞(M)-MDSC。肝细胞癌(HCC)中MDSC的主要亚型仍然难以捉摸。脾脏是人体最大的免疫器官,是许多细胞的起源。脾脏是否是MDSCs的起源仍是未知的。在这项研究中,我们调查了H22原位肝癌小鼠中主要MDSC亚型的表达,起源和动员。与M-MDSCs相比,PMN-MDSCs增加并在脾脏,外周血和肿瘤组织中占主导地位。脾切除术可以降低外周血和肿瘤组织中PMN-MDSC的百分比,增加外周血NK细胞的频率以及CD3 + CD4 + T,CD3 +肿瘤组织中的CD8 + T,NK和NKT细胞可减少肿瘤重量和腹水量,并延长肝癌小鼠的存活时间。荷瘤(TB)小鼠外周血趋化因子(CC基序)配体9(CCL9)和趋化因子(CC基序)配体2(CCL2)的水平升高,并且它们的受体CCR1和CCR2在脾PMN上表达-MDSC。迁移实验表明,CCL2和CCL9可以在体外吸引脾PMN-MDSCs。这些结果表明,原位H22肝癌小鼠中PMN-MDSCs增加并占优势,脾脏导致PMN-MDSCs的增加,并且CCL9和CCL2可以将PMN-MDSCs从脾脏中转移到外周血,从而促进肿瘤的发生。增长。

更新日期:2020-07-10
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