DEB-TACE与c-TACE治疗中晚期肝细胞癌的免疫微环境差异及TRADD介导Th17分化的机制

doi:10.13481/j.1671-587X.20260319

吉林大学学报(医学版) ›› 2026, Vol. 52 ›› Issue (3): 764-780.doi: 10.13481/j.1671-587X.20260319

DEB-TACE与c-TACE治疗中晚期肝细胞癌的免疫微环境差异及TRADD介导Th17分化的机制

曹耿飞¹,沙娅·玛哈提null²,顾俊鹏¹,纪卫政¹,阿斯哈尔·哈斯木null¹,任伟新¹()

^1.新疆医科大学第一附属医院介入放射科，新疆乌鲁木齐 830054
^2.新疆医科大学第一附属医院肿瘤中心，新疆乌鲁木齐 830054

收稿日期:2025-11-02 接受日期:2026-02-03 出版日期:2026-05-28 发布日期:2026-06-08
通讯作者: 任伟新 E-mail:rwx1031@163.com
作者简介:曹耿飞（1989-），男，山东省菏泽市人，主治医师，医学硕士，主要从事肝癌介入治疗方面的研究。
基金资助:
国家自然科学基金地区科学基金项目(32360189)

Differences in immune microenvironment between DEB-TACE and c-TACE in treatment of hepatocellular carcinoma and mechanism of TRADD-mediated Th17 differentiation

Gengfei CAO¹, SHAYA·Mahati²,Junpeng GU¹,Weizheng JI¹, ASIHAER·Hasimu¹,Weixin REN¹()

^1.Department of Interventional Radiology，First Affiliated Hospital，Xinjiang Medical University，Urumqi 830054，China
^2.Department of Oncology，First Affiliated Hospital，Xinjiang Medical University，Urumqi 830054，China

Received:2025-11-02 Accepted:2026-02-03 Online:2026-05-28 Published:2026-06-08
Contact: Weixin REN E-mail:rwx1031@163.com

摘要/Abstract

摘要：

目的探讨药物洗脱微球经动脉化疗栓塞（DEB-TACE）与传统经动脉化疗栓塞（c-TACE）治疗中晚期肝细胞癌（HCC）后局部免疫微环境的差异，阐明肿瘤坏死因子受体相关死亡结构域蛋白（TRADD）介导CD4⁺T淋巴细胞向17型辅助性T淋巴细胞（Th17）分化的可能机制。方法回顾性收集56例接受TACE治疗的中晚期HCC患者临床样本，分为DEB-TACE组和c-TACE组，每组28例。采用高通量RNA测序技术比较2组患者术前和术后HCC组织的基因表达谱及免疫细胞浸润丰度，流式细胞术分选2组患者HCC组织中的CD4⁺T淋巴细胞和Th17细胞，实时荧光定量PCR（RT-qPCR）法、Western blotting法和免疫荧光法检测细胞中TRADD及白细胞介素（IL）-23A等相关分子表达情况。体外分离活化原代CD4⁺T淋巴细胞，构建TRADD过表达（TRADD-OE）和敲低（TRADD-KD）模型，采用噻唑蓝（MTT）法检测各组CD4⁺ T淋巴细胞增殖活性，流式细胞术检测各组CD161⁺CCR6⁺ Th17细胞百分率，酶联免疫吸附试验（ELISA）法测定各组细胞上清液中IL-17水平，Western blotting法和RT-qPCR法检测各组细胞中Janus激酶（JAK）/信号转导与转录激活因子（STAT）信号通路关键蛋白磷酸化JAK-2（p-JAK2）、磷酸化STAT3（p-STAT3）蛋白表达水平以及下游转录因子芳香烃受体（AHR）和RAR相关孤儿受体γt（RORγt）mRNA及蛋白表达水平。联合使用JAK抑制剂（Ruxolitinib）干预TRADD-OE细胞，再次检测上述Th17细胞分化和信号通路指标。结果与c-TACE组比较，DEB-TACE组术后HCC组织中TRADD和IL-23A mRNA表达水平明显升高（P<0.05），且中央记忆CD4⁺T淋巴细胞和Th17细胞的浸润丰度明显升高。与c-TACE组比较，DEB-TACE组HCC组织中CD4⁺T淋巴细胞百分率明显升高（P<0.05），且分选出的CD4⁺T淋巴细胞和Th17细胞中TRADD和IL-23A mRNA及蛋白表达水平均明显升高（P<0.01）。与Con-OE组比较，TRADD-OE组CD4⁺T淋巴细胞增殖活性明显升高（P<0.01），CD161⁺CCR6⁺ Th17细胞百分率和上清中IL-17水平均明显升高（P<0.01），细胞中p-JAK2、p-STAT3、AHR和RORγt mRNA及蛋白表达水平均明显升高（P<0.01）；与Con-KD组比较，TRADD-KD组上述各项指标均明显降低（P<0.01）。JAK抑制剂干预后，与TRADD-OE组比较，TRADD-OE+JAK inhibitor组CD161⁺CCR6⁺ Th17细胞百分率和上清中IL-17水平均明显降低（P<0.01），细胞中CD161和CCR6蛋白荧光强度以及AHR和RORγt mRNA及蛋白表达水平均明显降低（P<0.01）。结论 DEB-TACE相较于c-TACE能更显著地重塑HCC局部免疫微环境并增加Th17细胞浸润，其作用机制可能与TRADD高表达并激活JAK/STAT信号通路，进而上调AHR和RORγt表达，促进CD4⁺T淋巴细胞向Th17细胞分化有关。

关键词: 肝细胞癌, 药物洗脱微球经动脉化疗栓塞, 免疫微环境, 肿瘤坏死因子受体相关死亡结构域蛋白, 17型辅助性T淋巴细胞, Janus激酶, 信号转导与转录激活因子

Abstract:

Objective To investigate the differences in the local immune microenvironment after drug-eluting bead transarterial chemoembolization （DEB-TACE） and conventional transarterial chemoembolization （c-TACE） for intermediate-advanced hepatocellular carcinoma （HCC）， and to clarify the possible mechanism by which tumor necrosis factor receptor-associated death domain （TRADD） mediates the differentiation of CD4⁺T lymphocytes into T helper 17 （Th17） lymphocytes. Methods The clinical samples from 56 patients with intermediate-advanced HCC who received TACE treatment were retrospectively collected and divided into DEB-TACE group and c-TACE group， with 28 cases in each group. High-throughput RNA sequencing was used to compare the changes in gene expression profiles and infiltration abundance of immune cells in HCC tissue before and after treatment in two groups. Flow cytometry was applied to sort CD4⁺T lymphocytes and Th17 cells from HCC tissues in two groups. The expressions of TRADD， interleukin （IL）-23A， and other related molecules in the cells were detected by real-time quantitative PCR （RT-qPCR） method， Western blotting method， and immunofluorescence method. The primary CD4⁺T lymphocytes were isolated and activated in vitro， and TRADD overexpression （TRADD-OE） and knockdown （TRADD-KD） models were constructed. The proliferation viability of CD4⁺T lymphocytes was detected by methytthiazolyl diphenyl-tetra zolilim（MTT） assay； the percentages of CD161⁺CCR6⁺ in Th17 cells in various group were detected by flow cytometry； the levels of IL-17 in the cell supernatant in various groups were measured by ELISA. The expression levels of key proteins of Janus kinase/signal transducer pathway and activator of transcription（STAT） signal phosphorylated-JAK2 （p-JAK2） and phosphorylated-STAT3 （p-STAT3） proteins and its downstream transcription factors aryl hydrocarbon receptor （AHR） and RAR-related orphan receptor gamma t （RORγt） mRNA and proteins were detected by Western blotting and RT-qPCR methods. The JAK inhibitor （Ruxolitinib） was used to intervene in TRADD-OE cells， and the aforementioned Th17 differentiation and signaling pathway indicators were detected again. Results Compared with c-TACE group， the expression levels of TRADD and IL-23A in post-operation HCC tissue in DEB-TACE group were significantly increased （P<0.05）， and the infiltration abundance of central memory CD4⁺T lymphocytes and Th17 cells was significantly increased. Compared with c-TACE group， the percentage of CD4⁺ T lymphocytes in HCC tissue in DEB-TACE group was significantly increased （P<0.05）， and the expression levels of TRADD and IL-23A mRNA and protein in the sorted CD4⁺T lymphocytes and Th17 cells were significantly increased （P<0.01）. Compared with Con-OE group， the proliferation activity of CD4⁺T lymphocytes in TRADD-OE group was significantly increased （P<0.01）； the of CD161⁺CCR6⁺ Th17 cells and the level of IL-17 in the supernatant were significantly increased （P<0.01）； the expression levels of p-JAK2， p-STAT3， AHR， and RORγt mRNA and proteins in the cells were all significantly increased （P<0.01）. Compared with Con-KD group， the above indicators in TRADD-KD group were all significantly decreased （P<0.01）. After intervention with JAK inhibitor， compared with TRADD-OE group， the percentage of CD161⁺CCR6⁺ Th17 cells and the level of IL-17 in the supernatant in TRADD-OE+JAK inhibitor group were significantly decreased （P<0.01）， and the fluorescence intensities of CD161 and CCR6， as well as the expression levels of AHR and RORγt mRNA and proteins in the cells， were significantly decreased （P<0.01）. Conclusion Compared with c-TACE， DEB-TACE can more significantly remodel the local immune microenvironment of HCC and increase Th17 cell infiltration. Its mechanism may be related to the high expression of TRADD and activating the JAK/STAT signaling pathway， thereby upregulating AHR and RORγt expressions and promoting the differentiation of CD4⁺T lymphocytes into Th17 cells.

Key words: Hepatocellular Carcinoma, Drug-eluting bead transarterial chemoembolization, Immune microenvironment, Tumor necrosis factor receptor-associated death domain, T helper 17 lymphocyte, Janus Kinase, Signal transducer and activator of transcription

中图分类号:

R735.7

曹耿飞,沙娅·玛哈提null,顾俊鹏,纪卫政,阿斯哈尔·哈斯木null,任伟新. DEB-TACE与c-TACE治疗中晚期肝细胞癌的免疫微环境差异及TRADD介导Th17分化的机制[J]. 吉林大学学报(医学版), 2026, 52(3): 764-780.

Gengfei CAO, SHAYA·Mahati,Junpeng GU,Weizheng JI, ASIHAER·Hasimu,Weixin REN. Differences in immune microenvironment between DEB-TACE and c-TACE in treatment of hepatocellular carcinoma and mechanism of TRADD-mediated Th17 differentiation[J]. Journal of Jilin University(Medicine Edition), 2026, 52(3): 764-780.

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Gene_ID	Cell type	Fold change	P value
AIM2	Activated CD4⁺T lymphocytes	20.368 553 210	0.013 000 638
PDCD1	T follicular helper cell	15.579 615 880	0.011 096 163
CLEC5A	Regulatory T lymphocytes	14.950 457 650	0.017 072 651
ANKRD22	Th17 cell	14.514 970 750	0.016 330 799
FASLG	Natural killer cell	13.856 520 250	0.015 023 090
HOXA1	CD56 bright natural killer cell	13.207 607 280	0.005 457 394
BCL11B	CD56 bright natural killer cell	11.030 248 040	0.011 544 782
KLRC1	Natural killer cell	10.429 241 360	0.038 653 619
CDH3	CD56 bright natural killer cell	9.706 281 760	0.015 512 624
CD70	Type 1 T helper cell	9.309 774 469	0.000 586 023
L1CAM	Regulatory T lymphocytes	9.298 367 003	0.006 524 248

Gene_ID	Cell type	Fold change	P value
ABHD3	Central memory CD4⁺T lymphocytes	1.299 519 371	0.031 902 364
ANK1	Th17 cell	15.934 043 830	5.156 56E-05
ANKRD22	Th17 cell	6.135 125 138	0.023 938 76
BZW2	Central memory CD4⁺T lymphocytes	1.475 780 042	0.012 213 002
CAMTA1	Th17 cell	1.103 822 788	0.026 864 438
CCDC65	Th17 cell	1.407 963 750	0.047 138 832
CD40	Th17 cell	1.621 074 362	0.017 409 637
CD63	Central memory CD4⁺T lymphocytes	1.306 966 557	0.000 565 941
ELMO2	Central memory CD4⁺T lymphocytes	1.442 394 442	0.025 307 557
IFT80	Th17 cell	1.486 992 324	0.023 311 561
IL17RA	Th17 cell	2.020 523 713	0.012 006 794
IL23A	Th17 cell	1.870 852 777	0.011 222 365
ITGB1	Central memory CD4⁺T lymphocytes	1.129 685 920	0.047 012 047
LSP1	Central memory CD4⁺T lymphocytes	2.381 922 808	0.030 755 375
SFXN3	Central memory CD4⁺T lymphocytes	1.909 800 611	0.002 226 840
STX4	Central memory CD4⁺T lymphocytes	1.432 307 982	0.005 207 203
TNIP2	Th17 cell	1.535 863 268	0.008 326 440
TRADD	Central memory CD4⁺T lymphocytes	1.701 717 402	0.007 064 042

Group	Cell type	TRADD mRNA	IL-23A mRNA	LSP1 mRNA	ITGB1 mRNA
c-TACE	CD4⁺T	0.83±0.07	0.58±0.02	0.94±0.05	1.04±0.05
	Th17	0.81±0.02	0.57±0.01	0.97±0.02	0.98±0.01
DEB-TACE	CD4⁺T	1.00±0.03^*	1.00±0.02^*	1.00±0.03	1.00±0.02
	Th17	1.01±0.06^*	0.99±0.05^*	0.98±0.05	0.97±0.04

Group	AHR mRNA	RORγt mRNA
Con-OE	1.00±0.06	1.00±0.10
Con-KD	1.08±0.10	1.05±0.10
TRADD-OE	2.98±0.01^*	1.52±0.06^*
TRADD-KD	0.63±0.05^△	0.88±0.12^△

Group	AHR mRNA	RORγt mRNA
Con-OE	1.01±0.11	1.01±0.13
TRADD-OE	1.56±0.23	1.64±0.13
Con-OE+JAK inhibitor	0.69±0.06^*	0.65±0.13^*
TRADD-OE+JAK inhibitor	1.25±0.12^△	1.13±0.11^△

DEB-TACE与c-TACE治疗中晚期肝细胞癌的免疫微环境差异及TRADD介导Th17分化的机制

Differences in immune microenvironment between DEB-TACE and c-TACE in treatment of hepatocellular carcinoma and mechanism of TRADD-mediated Th17 differentiation

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