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索拉非尼可防止晚期肝细胞癌肝硬化患者逃避宿主免疫。

Sorafenib prevents escape from host immunity in liver cirrhosis patients with advanced hepatocellular carcinoma.

作者信息

Nagai Hidenari, Mukozu Takanori, Matsui Daigo, Kanekawa Takenori, Kanayama Masahiro, Wakui Noritaka, Momiyama Kouichi, Shinohara Mie, Iida Kazunari, Ishii Koji, Igarashi Yoshinori, Sumino Yasukiyo

机构信息

Division of Gastroenterology and Hepatology, Toho University Medical Center, Omori Hospital, 6-11-1, Omorinishi, Ota-ku, Tokyo 143-8541, Japan.

出版信息

Clin Dev Immunol. 2012;2012:607851. doi: 10.1155/2012/607851. Epub 2012 May 14.

DOI:10.1155/2012/607851
PMID:22666283
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3359796/
Abstract

PURPOSE

It has been reported that Th2 cytokines downregulate antitumor immunity, while activation of type T cells promotes antitumor immunity. The aim of this paper was to evaluate host immunity in liver cirrhosis (LC) patients with advanced hepatocellular carcinoma (aHCC) receiving sorafenib therapy.

METHODS

Forty-five adult Japanese LC patients received sorafenib for aHCC between 2009 and 2011 at our hospital. Sorafenib was administered at a dose of 200-800 mg/day for 4 weeks. Blood samples were collected before and after treatment.

RESULTS

Eleven patients were treated with sorafenib at 200 mg/day (200 group), 27 patients received sorafenib at 400 mg/day (400 group), and 7 patients were given sorafenib at 800 mg/day (800 group). There was no significant change in the percentage of Th1 cells after treatment in any group. However, the percentages of Th2 cells and regulatory T cells were significantly decreased after treatment in the 400 group and 800 group compared with before treatment, although there was no significant change after treatment in the 200 group.

CONCLUSIONS

These results indicate that treatment with sorafenib might induce Th1 dominance and prevent the escape of tumor cells from the host immune system in LC patients with aHCC.

摘要

目的

据报道,Th2细胞因子会下调抗肿瘤免疫力,而T型细胞的激活则会促进抗肿瘤免疫力。本文旨在评估接受索拉非尼治疗的晚期肝细胞癌(aHCC)肝硬化(LC)患者的宿主免疫力。

方法

2009年至2011年期间,45名成年日本LC患者在我院接受了索拉非尼治疗aHCC。索拉非尼以200 - 800毫克/天的剂量给药,持续4周。在治疗前后采集血样。

结果

11名患者接受200毫克/天的索拉非尼治疗(200组),27名患者接受400毫克/天的索拉非尼治疗(400组),7名患者接受800毫克/天的索拉非尼治疗(800组)。任何一组治疗后Th1细胞百分比均无显著变化。然而,与治疗前相比,400组和800组治疗后Th2细胞和调节性T细胞百分比显著降低,而200组治疗后无显著变化。

结论

这些结果表明,索拉非尼治疗可能会诱导Th1优势,并防止aHCC的LC患者肿瘤细胞从宿主免疫系统中逃逸。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cc2/3359796/bee062c4745f/CDI2012-607851.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cc2/3359796/b2b846816612/CDI2012-607851.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cc2/3359796/bee062c4745f/CDI2012-607851.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cc2/3359796/b2b846816612/CDI2012-607851.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cc2/3359796/bee062c4745f/CDI2012-607851.009.jpg

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Semin Liver Dis. 2010 Feb;30(1):52-60. doi: 10.1055/s-0030-1247132. Epub 2010 Feb 19.
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Sorafenib inhibits the shedding of major histocompatibility complex class I-related chain A on hepatocellular carcinoma cells by down-regulating a disintegrin and metalloproteinase 9.索拉非尼通过下调解整合素金属蛋白酶 9 抑制肝癌细胞主要组织相容性复合体 I 相关链 A 的脱落。
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Instability of the transcription factor Foxp3 leads to the generation of pathogenic memory T cells in vivo.
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Kaohsiung J Med Sci. 2021 Oct;37(10):894-902. doi: 10.1002/kjm2.12413. Epub 2021 Jun 24.
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Direct and Indirect Modulation of T Cells by VEGF-A Counteracted by Anti-Angiogenic Treatment.VEGF-A 对 T 细胞的直接和间接调节作用可被抗血管生成治疗拮抗。
Front Immunol. 2021 Mar 29;12:616837. doi: 10.3389/fimmu.2021.616837. eCollection 2021.
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