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The Galectin-9/Tim-3 pathway is involved in the regulation of NK cell function at the maternal-fetal interface in early pregnancy

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Cellular & Molecular Immunology 2016年第1期13卷 73-81页

作者： Yan-Hong Li Wen-Hui Zhou Yu Tao Song-Cun Wang Yun-lan Jiang Di Zhang hai-lan piao Qiang Fu Da-Jin Li Mei-Rong Du Laboratory for Reproductive Immunology Hospital and Institute of Obstetrics and Gynecology Fudan University Shanghai Medical College Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases Shanghai China Medical Center for Human Reproduction Beijing Chaoyang HospitalCapital Medical University Beijing China Maternal and Child Care Hospital Of Huangpu District Shanghai China These authors contributed equally to this work

Decidual natural killer （dNK） cells actively participate in the establishment and maintenance of maternal-fetal immune tolerance and act as local guardians against infection. However, how dNK cells maintain the immune balance between tolerance and anti-infection immune responses during pregnancy remains unknown. Here, we demonstrated that the inhibitory molecule T-cell immunoglobulin domain and mucin domain-containing molecule-3 （Tim-3） are expressed on over 60% of dNK cells. Tim-3^＋ dNK cells display higher interleukin （IL）-4 and lower tumor necrosis factor （TNF）-α and perforin production. Human trophoblast cells can induce the transformation of peripheral NK cells into a dNK-like phenotype via the secretion of galectin-9 （Gal-9） and the interaction between Gal-9 and Tim-3. In addition, trophoblasts inhibit lipopolysaccharide （LPS）-induced pro-inflammatory cytokine and perforin production by dNK cells, which can be attenuated by Tim-3 neutralizing antibodies. Interestingly, a decreased percentage of Tim-3-expressing dNK cells were observed in human miscarriages and murine abortion-prone models. Moreover, T helper （Th）2-type cytokines were decreased and Thl-type cytokines were increased in Tim-3^＋ but not Tim-3- dNK cells from human and mouse miscarriages. Therefore, our results suggest that the Gal-9/Tim-3 signal is important for the regulation of dNK cell function, which is beneficial for the maintenance of a normal pregnancy.

关键词： cytotoxicity galectin-9/Tim-3 NK cells pregnancy Th2

The CXCL12/CXCR4 axis is involved in the maintenance of Th2 bias at the maternal/fetal interface in early human pregnancy

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Cellular & Molecular Immunology 2012年第5期9卷 423-430页

作者： hai-lan piao Yu Tao Rui Zhu Song-Cun Wang Chuan-Ling Tang Qiang Fu Mei-Rong Du Da-Jin Li Laboratory for Reproductive Immunology Hospital and Institute of Obstetrics and GynecologyFudan University Shanghai Medical CollegeShanghai 200011China Department of Obstetrics and Gynecology The First Affiliated Hospital of Sochow UniversitySuzhou 215006China Department of Immunology Binzhou Medical UniversityYantai 264003China

The regulatory mechanism of Th2 bias at the maternal/fetal interface remains unclear. In this study, we characterized cytokine production in decidual stromal cells （DSCs）, decidual immune cells （DICs） and embryo-derived trophoblast cells, and investigated the regulation of CXCL12/CXCR4 interaction on Th2 bias at the maternal/fetal interface in early human pregnancy. We found differential production of Th 1-type and Th2-type cytoki nes by trophoblasts, DSCs and DICs. The secretion of these cytokines varied in different cell cocultures, conduced to Th2 bias. Flow cytometry showed that coculture of trophoblasts with DSCs and DICs significantly increased IL-4 and IL-IO production in trophoblasts, and IL-IO production in DSCs. However, the coculture of trophoblasts with DSCs and DICs significantly increased interferon （IFN）-7 expression in DSCs, and tumor-necrosis factor （TNF）-a expression in DICs. No change was seen in Thl-type cytokine production in trophoblasts, and in Th2-type cytokine production in DICs in all cocultures. Furthermore, pre-treatment with anti-CXCR4 neutralizing antibody upregulated the production of the Thl-type cytokines IFN-y and TNF-a, and downregulated the production of the Th2-type cytokines IL-4 and IL-IO, in trophoblasts, DSCs, DICs or their cocultures. Interestingly, rhCXCL12 inhibited production of the Thl-type cytokine TNF-a and enhanced the expression of the Th2-type cytokines such as IL-4 and IL-IO in DICs; this effect was abrogated by anti-CXCR4 antibody. Our present study has elucidated the individual contributions of component cells to the shaping of Th2 bias, and uncovered a complicated cross-talk viathe CXCL12/CXCR4 signal at the maternal/fetal interface in early human pregnancy.

关键词： CXCL12/CXCR4 maternal/fetal interface Thl/Th2

Immunotoxin Therapy for Lung Cancer

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Chinese Medical Journal 2017年第5期130卷 607-612页

作者： Li-Yi Xie hai-lan piao Min Fan Zhen Zhang Chen Wang Darell D Bigner Xu-Hui Bao Department of Radiation Oncology Fudan University Shanghai Cancer Center Shanghai 200032 China Department of Oncology Shanghai Medical College Fudan University Shanghai 200032 China Department of Pathology Duke University Medical Center Durham North Carolina USA Department of Medicine China-Japan Friendship Hospital Beijing 100029 China

INTRODUCTIONLung cancer is the leading cause for cancer-related deaths in both genders throughout the world. In the United States alone, there were 224,390 estimated new lung cancer cases and 158,080 estimated deaths ... 详细信息

关键词： Immunotherapy Immunotoxins Lung Neoplasms Molecular Targeted Therapy

CD56^brightCD25^＋ NK cells are preferentially recruited to the maternal/fetal interface in early human pregnancy

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Cellular & Molecular Immunology 2015年第1期12卷 77-86页

作者： Yu Tao Yan-Hong Li hai-lan piao Wen-Jie Zhou Di Zhang Qiang Fu Song-Cun Wang Da-Jin Li Mei-Rong Du Laboratory for Reproductive Immunology Hospital and Institute of Obstetrics and Gynecology Fudan University Shanghai Medical College Shanghai KeyLaboratory of Female Reproductive Endocrine Related Diseases Shanghai China

Decidual natural killer （dNK） cells are believed to be critical for maintaining maternal/fetal tolerance and regulating placental vascular remodeling based upon their abundance and unique phenotype during early pregnancy. However, the mechanism for how the dNK cells play such important roles in successful pregnancy remains undefined. Here, we identified a subtype of dNK cells characterized as having a CD3-CD56^brightCD25^＋ phenotype. We found that CD56^brightCD25^＋ NK cells preferentially localize to the maternal/fetal interface during early human pregnancy. CD25^＋ dNK cells account for approximately 75% of CD25-expressing decidual immune cells （DICs）. However, less than 5% of CD25-positive peripheral blood mononuclear cells are CD25^＋ NK cells. Furthermore, CD25^＋ and CD25^- dNK cells exhibit distinct phenotypes： CD25^＋ dNK cells display a more activated phenotype and greater cytokine-secreting capacity. Interestingly, coculture of peripheral NK （pNK） cells with primary trophoblasts upregulates the percentage of CD25-expressing pNK cells, resulting in increased expression of activation markers and cytokine production by pNK cells. In addition, we demonstrated that the CXCL12/CXCR4 axis is crucial for the recruitment of CD25^＋ dNK cells and contributes to the accumulation of CD3^-CD56^brightCD25^＋ dNK cells at the maternal/fetal interface. Thus, our data reveal that the crosstalk between trophoblasts and pNK cells leads to the accumulation of CD3^-CD56^brightCD25^＋ dNK cells, which exert a regulating effect at the maternal/fetal interface.

关键词： CXCL12/CXCR4 CD3^-CD56^brightCD25^+ N K cells maternal/fetal interface trophoblasts

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毛囊类器官研究:现状、问题与前景

中国组织工程研究 2025年第31期29卷 6733-6742页

作者：王钊龚琳朴永君大连医科大学附属第一医院皮肤科辽宁省大连市116000

背景:毛囊体外重建依赖于毛乳头细胞及角质形成细胞3D共培养时的自组装行为,该过程与毛囊胚胎发育极为相似,因此,毛囊类器官可作为毛囊再生相关基础研究良好的体外模型,目前,通过仿生系统培养的全人源毛囊类器官已能成功移植到动物体内... 详细信息

背景:毛囊体外重建依赖于毛乳头细胞及角质形成细胞3D共培养时的自组装行为,该过程与毛囊胚胎发育极为相似,因此,毛囊类器官可作为毛囊再生相关基础研究良好的体外模型,目前,通过仿生系统培养的全人源毛囊类器官已能成功移植到动物体内。毛囊类器官研究使毛囊再生成为可能,但构建方法亦无统一定论,仍面临诸多挑战。目的:综述目前毛囊类器官的研究进展,总结毛囊类器官培养方法及表征,阐述应用前景,为后续研究提供可靠依据,以期促进其在组织工程及脱发治疗的临床转化。方法:应用计算机在中国知网(CNKI)及PubMed数据库中,以“毛囊再生,毛发再生,类器官”为中文检索词,“hair growth,hair loss,hair regeneration,hair follicle,dermal papilla cell,organoid”为英文检索词进行检索,查阅国内外关于毛囊类器官的相关文献,共纳入文献67篇进行后续分析。结果与结论:①不同来源的毛乳头细胞与角质形成细胞可在体外构建毛囊类器官,以获得鼠源、人-鼠嵌合及人源毛囊类器官,并成功用于啮齿动物移植模型;②多种重编程方法如电刺激、添加重组蛋白、解离细胞基因过表达等可用于促进毛囊类器官毛胚形成及毛钉伸长,同时,多种3D打印技术的应用已实现大小可控毛囊类器官的批量生产,极大提高了生产效率;③在解离细胞共培养体系中加入黑素细胞时,或可破译新生毛囊的色素缺失难题,而加入人脐静脉血管内皮细胞时,细胞聚集体内的新生血管可改善营养供给,减少中心部位坏死;④随着工程化类毛囊技术逐渐趋于成熟,患者自体细胞构建的毛囊类器官或可用于严重脱发的个体化医疗。

关键词：脱发毛囊再生毛乳头细胞毛囊类器官上皮-间充质交互作用 3D培养类器官组织工程工程化类器官

Ribavirin and IFN-α combination therapy induces CD4+ T-cell proliferation and Th1 cytokine secretion in patients with chronic hepatitis B

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World Journal of Gastroenterology 2007年第41期13卷 5440-5445页

作者： Fen-Yu Ren hai Jin Xi-Xu piao Feng-Shun piao Department of Gastroenterology and Hepatology Yanbian University Hospital Yanji 133000 Jilin Province China

AIM: To investigate the anti-viral mechanism of combination therapy of interferon (IFN)-α and ribavirin in patients with chronic hepatitis B. METHODS: Twenty patients were assigned to receive either IFN-α plus ribavirin (group A,n = 14) or no treatment as a control (group B,n = 6). Patients were analyzed for T-cell proliferative responses specific for hepatitis B virus (HBV)-antigen and cytokine production by peripheral blood mononuclear cells (PBMCs). RESULTS: Combination therapy induced HBV-antigen specific CD4+ T-cell proliferative responses in four patients (28.6%). Production of high levels of HBV-specific IFN-γ,tumor necrosis factor (TNF)-α,interleukin (IL)-12 by PBMCs was found in five patients (35.7%),who showed significantly lower HBV DNA levels in serum at 12 mo after treatment ended (P = 0.038) and at 24 mo of follow-up (P = 0.004) than those without high levels of cytokine production. CONCLUSION: HBV-antigen specific CD4+ T cells may directly control HBV replication and secretion of anti-viral T helper 1 (Th1) cytokines by PBMCs during combination therapy of chronic hepatitis B with ribavirin and IFN-α.

关键词： Hepatitis B Interferon-alpha Ribavirin CD4+ T cells Th1

Dichloroacetic acid and rapamycin synergistically inhibit tumor progression

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2023年第5期24卷 397-405页

作者： Huan CHEN Kunming LIANG Cong HOU hai-long piao CAS Key Laboratory of Separation Science for Analytical Chemistry Dalian Institute of Chemical PhysicsChinese Academy of SciencesDalian 116023China Department of Biochemistry&Molecular Biology School of Life SciencesChina Medical UniversityShenyang 110122China University of Chinese Academy of Sciences Beijing 100049China

Mammalian target of rapamycin(mTOR)controls cellular anabolism,and mTOR signaling is hyperactive in most cancer *** a result,inhibition of mTOR signaling benefits cancer *** is a US Food and Drug Administration(FDA)-approved drug,a specific mTOR complex 1(mTORC1)inhibitor,for the treatment of several different types of ***,rapamycin is reported to inhibit cancer growth rather than induce *** dehydrogenase complex(PDHc)is the gatekeeper for mitochondrial pyruvate *** inactivation has been observed in a number of cancer cells,and this alteration protects cancer cells from senescence and nicotinamide adenine dinucleotide(NAD^(+))*** this paper,we describe our finding that rapamycin treatment promotes pyruvate dehydrogenase E1 subunit alpha 1(PDHA1)phosphorylation and leads to PDHc inactivation dependent on mTOR signaling inhibition in *** inactivation reduces the sensitivity of cancer cells'response to *** a result,rebooting PDHc activity with dichloroacetic acid(DCA),a pyruvate dehydrogenase kinase(PDK)inhibitor,promotes cancer cells'susceptibility to rapamycin treatment in vitro and in vivo.

关键词： Dichloroacetic acid(DCA) Rapamycin Pyruvate dehydrogenase E1 subunit alpha 1(PDHA1) Mammalian target of rapamycin(mTOR)

Long noncoding RNA NALT1-induced gastric cancer invasion and metastasis via NOTCH signaling pathway

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World Journal of Gastroenterology 2019年第44期25卷 6508-6526页

作者： hai-Yan piao Shuai Guo Yue Wang Jun Zhang Medical Oncology Department of Gastrointestinal Cancer Liaoning Province Cancer Hospital&Institute(Cancer Hospital of China Medical University)Shenyang 110042Liaoning ProvinceChina Gastric Cancer Department Liaoning Province Cancer Hospital&Institute(Cancer Hospital of China Medical University)Shenyang 110042Liaoning ProvinceChina

BACKGROUNDLong noncoding RNAs (lncRNAs) are aberrant and play critical roles in gastriccancer (GC) progression and metastasis. Searching for coexpressed lncRNAclusters or representative biomarkers related to malignant phenotypes of GC mayhelp to elucidate the mechanism of tumor development and predict the prognosisof *** investigate the prognostic value of NOTCH1 associated with lncRNA in T cellacute lymphoblastic leukemia 1 (NALT1) in GC and the mechanism of itsinvolvement in GC invasion and *** sequencing and corresponding clinical data were downloaded from TheCancer Genome Atlas database. The significance module was studied byweighted gene coexpression network analysis. A total of 336 clinical sampleswere included in the study. Gene silencing, reverse transcription polymerasechain reaction, western blotting, scrape motility assay, and Transwell migrationassay were used to assess the function of *** the transcriptome level, 3339 differentially expressed lncRNAs were *** gene coexpression network analysis was used to obtain 15 lncRNAclusters and observe their coexpression. Pearson’s correlation showed that blue module was correlated with tumor grade and survival. NALT1 was the hublncRNAof blue module and was an independent risk factor for GC ***1 was overexpressed in GC and its expression was closely related toinvasion and metastasis. The mechanism may involve NALT1 regulation ofNOTCH1, which is associated with lncRNA in T cell acute lymphoblasticleukemia, through cis regulation, thereby affecting the expression of the NOTCHsignaling ***1 is overexpressed and promotes invasion and metastasis of GC. Themechanism may be related to regulation of NOTCH1 by NALT1 and its effect onNOTCH signaling pathway expression.

关键词： Gastric cancer Weighted gene coexpression network analysis NALT1 NOTCH1 Cancer survival

Silencing of signal transducer and activator of transcription 3 expression by RNA interference suppresses growth of human hepatocellular carcinoma in tumor-bearing nude mice

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World Journal of Gastroenterology 2009年第21期15卷 2602-2608页

作者： Jing Li Yun-Feng piao Zheng Jiang Li Chen hai-Bo Sun Department of Gastroenterology the First Affiliated Hospital of Liaoning Medical University Jinzhou 121000 Liaoning Province China Department of Gastroenterology the First Hospital of Jilin University Changchun 130021 Jilin Province China Department of Orthopedics the Second Hospital of Jinzhou City Jinzhou 121003 Liaoning Province China

AIM： To explore the effect of silencing of signal transducer and activator of transcription 3 （STAT3） expression by RNA interference （RNAi） on growth of human hepatocellular carcinoma （HCC） in tumorbearing nude mice in vivo.METHODS： To construct the recombinant plasmid of pSilencer 3.0-H1-STAT3-siRNA-GFP （pSHI-siRNA- STAT3） and establish the tumor-bearing nude mouse model of the HCC cell line SMMC7721, we used intratumoral injection together with electroblotting to transfect the recombinant plasmid pSHI-siRNA- STAT3 into the transplanted tumor. The weight of the nude mice and tumor volumes were recorded. STAT3 gene transcription was detected by semi-quantitative reverse transcription polymerase chain reaction （RT- PCR）. Level of protein expression and location of STAT3 were determined by Western blotting and immunohistochemical staining. STAT3-related genes such as survivin, c-myc, VEGF, p53 and caspase3 mRNA and protein expression were detected in tumor tissues at the same time. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） assay was used to detect apoptosis of tumor cells.RESULTS： The weight of the treated nude mice increased, and the tumor volume decreased markedly compared with those of the mock-treated and negative control groups （P 〈 0.01）. The results of RT-PCR and Western blotting showed that mRNA and protein levels of STAT3 declined markedly in the treated group. The change in STAT3-related gene expression in tumor tissues at the mRNA and protein level also varied, the expression of survivin, VEGF and c-myc were obviously reduced, and expression of p53 and caspase3 increased （P 〈 0.01）. Most of the tumor tissue ceils in the treated group developed apoptosis that was detected by TUNEL assay.CONCLUSION： Silencing of STAT3 expression by RNAi significantly inhibits expression of STAT3 mRNA and protein, and suppresses growth of human HCC in tumor-bearing nude mice. The mechanism may be related to down-regulation of survi

关键词： RNA interference Signal transducerand activator of transcription 3 transcription factor Hepatocellular carcinoma Xenograft model antitumorassays Nude mouse