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| 1 | Transplantation of Human Bone Marrow Mesenchymal Stem Cell Ameliorates the Autoimmune Pathogenesis in MRL/lpr Mice显示文摘Recent evidence indicates that mesenchymal stem cells (MSC) possess immunosuppressive properties both in vitro and in vivo. We previously demonstrated the functional abnormality of bone marrow derived MSC in patients with systemic lupus erythematosus (SLE). In this study, we aimed to investigate whether transplantation of human bone marrow derived MSC affects the autoimmune pathogenesis in MRL/lpr mice. We found that human MSC from healthy donors reduced the proliferation of T lymphocytes from MRL/lpr mice in a dose-dependent fashion. Two weeks after in vivo transfer of MSC, we detected significantly reduced serum levels of anti ds-DNA antibodies and 24 hour proteinuria in MRL/lpr mice as compared with control groups without MSC transplantation. Moreover, flow cytometric analysis revealed markedly reduced number of CD4+ T cells while increased Th1 subpopulation in MSC group and MSC + CTX group when compared with controls. Histopathological examination showed significantly reduced renal pathology in MSC-treated mice. Immunohistochemical studies further revealed reduced expression of TGF-β, FN, VEGF and the deposition of complement C3 in renal tissue after MSC and MSC + CTX treatment. Taken together, we have demonstrated that transplantation of human MSC can significantly inhibit the autoimmune progression in MRL/lpr mice. | Kangxing Zhou Huayong Zhang Ouyang Jin Xuebing Feng Genhong Yao Yayi Hou Lingyun Sun | 2008 | Cellular & Molecular Immunology2008，5，6： | 59 |
| 2 | The regulation of the Treg/Th 17 balance by mesenchyma stem cells in human systemic lupus erythematosus显示文摘 | Dandan Wang Saisai Huang Xinran Yuan Jun Liang Renju Xu Genhong Yao Xuebing Feng Lingyun Sun | 2017 | Cellular & Molecular Immunology2017，14，5： | 44 |
| 3 | PLP2, a potent deubiquitinase from murine hepatitis virus, strongly inhibits cellular type I interferon production显示文摘由象严重急性呼吸症候群(SARS ) 那样的 coronaviruses 的感染 coronavirus (SCoV ) 和老鼠肝炎病毒 A59 (MHV-A59 ) 导致很小的类型我干扰素(IFN ) 生产由招待细胞,它为与 SARS 联系的快速的病毒的生长和严重 immunopathology 潜在地负责。然而,为在感染 coronaviruses 的房间的低 IFN 生产的分子的机制仍然保持不清楚。这里,我们提供证据象 Papain 一样朊酶领域 2 (PLP2 ) , nonstructural 蛋白质的一个催化领域 3 (nsp3 ) MHV-A59,能绑在 IRF3,引起它的 deubiquitination 并且阻止它的原子 translocation。作为后果, PLP2 的合作表示强烈禁止 CARDIF- ,调停 TBK1 、调停 IRF3 的 IFN 记者活动。另外,我们显示出那野类型的 PLP2 然而并非缺乏 deubiquitinase 的变异的 PLP2 (称) 活动能减少感应的 IFN 并且在感染 VSV 的房间支持病毒的生长。因此,我们的学习揭开了一病毒称它 coronaviruses 可以使用逃离主人天生的抗病毒的回答。 | Dahai Zheng Gang Chen Beichu Guo Genhong Cheng Hong Tang | 2008 | Cell Research2008，18，11： | 20 |
| 4 | Role of tumor microenvironment in triple-negative breast cancer and its prognostic significance显示文摘Breast cancer has been shown to live in the tumor microenvironment, which consists of not only breast cancer cells themselves but also a significant amount of pathophysiologically altered surrounding stroma and cells. Diverse components of the breast cancer microenvironment, such as suppressive immune cells, re-programmed fibroblast cells, altered extracellular matrix(ECM) and certain soluble factors, synergistically impede an effective anti-tumor response and promote breast cancer progression and metastasis. Among these components, stromal cells in the breast cancer microenvironment are characterized by molecular alterations and aberrant signaling pathways,whereas the ECM features biochemical and biomechanical changes. However, triple-negative breast cancer(TNBC), the most aggressive subtype of this disease that lacks effective therapies available for other subtypes, is considered to feature a unique microenvironment distinct from that of other subtypes, especially compared to Luminal A subtype. Because these changes are now considered to significantly impact breast cancer development and progression, these unique alterations may serve as promising prognostic factors of clinical outcome or potential therapeutic targets for the treatment of TNBC. In this review, we focus on the composition of the TNBC microenvironment, concomitant distinct biological alteration, specific interplay between various cell types and TNBC cells, and the prognostic implications of these findings. | Tianjian Yu Genhong Di | 2017 | Chinese Journal of Cancer Research2017，29，3： | 17 |
| 5 | MicroRNA-663 induces immune dysregulation by inhibiting TGF-β1 production in bone marrow-derived mesenchymal stem cells in patients with systemic lupus erythematosus显示文摘Mesenchymal stem cells(MSCs)are critical for immune regulation.Although several microRNAs(miRNAs)have been shown to participate in autoimmune pathogenesis by affecting lymphocyte development and function,the roles of miRNAs in MSC dysfunction in autoimmune diseases remain unclear.Here,we show that patients with systemic lupus erythematosus(SLE)display a unique miRNA signature in bone marrow-derived MSCs(BMSCs)compared with normal controls,among which miR-663 is closely associated with SLE disease activity.MiR-663 inhibits the proliferation and migration of BMSCs and impairs BMSC-mediated downregulation of follicular T helper(Tfh)cells and upregulation of regulatory T(Treg)cells by targeting transforming growth factorβ1(TGF-β1).MiR-663 overexpression weakens the therapeutic effect of BMSCs,while miR-663 inhibition improves the remission of lupus disease in MRL/lpr mice.Thus,miR-663 is a key mediator of SLE BMSC regulation and may serve as a new therapeutic target for the treatment of lupus. | Linyu Geng Xiaojun Tang Kangxing Zhou Dandan Wang Shiying Wang Genhong Yao Weiwei Chen Xiang Gao Wanjun Chen Songtao Shi Nan Shen Xuebing Feng Lingyun Sun | 2019 | Cellular & Molecular Immunology2019，16，3： | 16 |
| 6 | Type I IFN augments IL-27-dependent TRIM25 expression to inhibit HBV replication显示文摘Hepatitis B virus(HBV)can cause chronic hepatitis B,which may lead to cirrhosis and liver cancer.Type I interferon(IFN)is an approved drug for the treatment of chronic hepatitis B.However,the fundamental mechanisms of antiviral action by type I IFN and the downstream signaling pathway are unclear.TRIM25 is an IFN-stimulated gene(ISG)that has an important role in RIG-I ubiquitination and activation.Whether TRIM25 is induced in liver cells by type I IFN to mediate anti-HBV function remains unclear.Here we report that interleukin-27(IL-27)has a critical role in IFN-induced TRIM25 upregulation.TRIM25 induction requires both STAT1 and STAT3.In TRIM25 knockout HepG2 cells,type I IFN production was consistently attenuated and HBV replication was increased,whereas overexpression of TRIM25 in HepG2 cells resulted in elevated IFN production and reduced HBV replication.More interestingly,we found that TRIM25 expression was downregulated in HBV patients and the addition of serum samples from HBV patients could inhibit TRIM25 expression in HepG2 cells,suggesting that HBV might have involved a mechanism to inhibit antiviral ISG expression and induce IFN resistance.Collectively,our results demonstrate that type I IFN-induced TRIM25 is an important factor in inhibiting HBV replication,and the IFN-IL-27-TRIM25 axis may represent a new target for treating HBV infection. | Guangyun Tan Qingfei Xiao Hongxiao Song Feng Ma Fengchao Xu Di Peng Na Li Xiaosong Wang Junqi Niu Pujun Gao F Xiao-Feng Qin Genhong Cheng | 2018 | Cellular & Molecular Immunology2018，15，3： | 13 |
| 7 | Coronavirus MHV-A59 infects the lung and causes severe pneumonia in C57BL/6 mice显示文摘It remains challenging to develop animal models of lung infection and severe pneumonia by severe acute respiratory syndrome coronavirus(SARS-CoV) and Middle East respiratory syndrome cornavirus(MERS-Co V) without high level of containment. This inevitably hinders understanding of virushost interaction and development of appropriate countermeasures. Here we report that intranasal inoculation of sublethal doses of murine coronavirus mouse hepatitis virus A-59(MHV-A59), a hepatic and neuronal tropic coronavirus, can induce acute pneumonia and severe lung injuries in C57BL/6 mice. Inflammatory leukocyte infiltrations, hemorrhages and fibrosis of alveolar walls can be observed 2-11 days after MHV-A59 infection. This pathological manifestation is associated with dramatical elevation of tissue IP-10 and IFN-γ and moderate increase of TNF-α and IL-1β, but inability of anti-viral type I interferon response. These results suggest that intranasal infection of MHV-A59 would serve as a surrogate mouse model of acute respiratory distress syndrome by SARS-CoV and MERS-CoV infections. | Zhangsheng Yang Jun Du Gang Chen Jie Zhao Xuanming Yang Lishan Su Genhong Cheng Hong Tang | 2014 | Virologica Sinica2014，29，6： | 9 |
| 8 | Gene Expression Profiling in Apoptotic K562 Cells Treated by Homoharringtonine显示文摘基因薄片技术被用来在 homoharringtonine 导致的 apoptotic K562 房间决定基因表达侧面。mRNAs 被发现显著地被换掉的 44 的表达式在与能够同时检测 14,218 不同人的 mRNA 种类的一块基因芯片屏蔽以后被识别。这些基因, 17 是起来调整的, 27 是下面调整的。他们中的大多数被发现与 apoptosis, oncogenes,或肿瘤抑制有关。有改变的基因表达的几基因,例如人的转变生长因素贝它可诱导的早蛋白质基因( TIEG ),在调整蛋白质上面的 维生素 D3 1 基因( VDUP1 ), RNA 有约束力的主题蛋白质 4 基因( RBM4 )和 v-myc myelocytomatosis 病毒的癌基因相当或相同的事物( C-MYC ),被RNA 印迹分析证实。根据在这些 apoptotic 房间的动态基因表达模式,激活的转变生长因素贝它和肿瘤坏死因素发信号小径在导致 homoharringtonine 的 apoptosis 起一个重要作用。TIEG 显著地在 apoptosis 正式就职以后被改变,它应该为 apoptosis 信号传播是批评的。 | Wei JINX Jiong WU Zhigang ZHUANG Junjie Li Fei FEI Genhong DI Ying CHEN Ming YAO Zhimin SHAO | 2007 | Acta Biochimica et Biophysica Sinica2007，39，12： | 6 |
| 9 | Structural analysis of asparaginyl endopeptidase reveals the activation mechanism and a reversible intermediate maturation stage显示文摘Asparaginyl endopeptidase (AEP ) 是有为在 P1 地点的天门冬素残余的偏爱的 endo/lysosomal 半胱氨酸 endopeptidase 并且在像使用费的受体 3/7/9 的成熟起一个重要作用。AEP 被知道为催化激活在酸的 pH 经历 autoproteolytic 成熟。这里,我们描述 AEP 酶原的水晶结构和 AEP 的成熟形式。在 AEP 和 caspases 之间的结构的比较在关键残余的作文并且在催化机制揭示了类似。Mutagenesis 研究作为为肽底层的劈开是必要的残余识别了 N44, R46, H150, E189, C191, S217/S218 和 D233。在成熟期间, AEP 的帽子领域的 autoproteolytic 劈开在核心领域上开创存取到活跃地点。出人意料地,一个中间的 autoproteolytic 成熟阶段被发现在近似 pH 4.5 在哪个部分激活的 AEP 能被颠倒回到它的酶原形式。这个唯一的特征被 AEP pH4.5 (AEP 在 pH 被成熟 4.5 并且在 pH 结晶 8.5 ) ,在哪个破肽契约被重新绑扎,结构被转变回到它的酶原形式。另外, AEP 禁止者 cystatin C 能被充分激活的 AEP 消化,但是不能被激活的组织蛋白酶消化。因此,我们第一次证明 cystatins 可以为活跃地点通过底层竞争调整 AEP 的活动。 | Lixia Zhao Tian Hua Christopher Crowley Heng Ru Xiangmin Ni Neil Shaw Lianying Jiao Wei Ding Lu Qu Li-Wei Hung Wei Huang Lei Liu Keqiang Ye Songying Ouyang Genhong Cheng Zhi-Jie Liu | 2014 | Cell Research2014，24，3： | 6 |
| 10 | Crystal structure of the ubiquitin-like domain of human TBK1显示文摘TANK-binding kinase 1(TBK1)is an important enzyme in the regulation of cellular antiviral effects.TBK1 regulates the activity of the interferon regulatory factors IRF3 and IRF7,thereby playing a key role in type I interferon(IFN)signaling pathways.The structure of TBK1 consists of an N-terminal kinase domain,a middle ubiquitin-like domain(ULD),and a C-terminal elongated helical domain.It has been reported that the ULD of TBK1 regulates kinase activity,playing an important role in signaling and mediating interactions with other molecules in the IFN pathway.In this study,we present the crystal structure of the ULD of human TBK1 and identify several con-served residues by multiple sequence alignment.We found that a hydrophobic patch in TBK1,containing residues Leu316,Ile353,and Val382,corresponding to the“Ile44 hydrophobic patch”observed in ubiquitin,was conserved in TBK1,IκB kinase epsilon(IKKε/IKKi),IκB kinase alpha(IKKα),and IκB kinase beta(IKKβ).In com-parison with the structure of the IKKβULD domain of Xenopus laevis,we speculate that the Ile44 hydrophobic patch of TBK1 is present in an intramolecular binding surface between ULD and the C-terminal elongated heli-ces.The varying surface charge distributions in the ULD domains of IKK and IKK-related kinases may be relevant to their specificity for specific partners. | Jian Li Jun Li Andrea Miyahira Jian Sun Yingfang Liu Genhong Cheng Huanhuan Liang | 2012 | Protein & Cell2012，3，5： | 5 |
| 11 | Structural basis for termination of AIM2-mediated signaling by p202显示文摘 | Heng Ru Xiangmin Ni LixiaZhao Christopher Crowle Wei Ding Li-Wei Hung Neil Shaw Genhong Cheng Zhi-Jie Liu | 2013 | Cell Research2013，23，6： | 5 |
| 12 | Crystal structure and nucleotide selectivity of human IFIT5/ISG58显示文摘 | Feng Feng LingminYuan Yao E Wang Christopher Crowley Zongyang Lv Jingjing Li Yingfang Liu Genhong Cheng Su Zeng Huanhuan Liang | 2013 | Cell Research2013，23，8： | 4 |
| 13 | Biocompatibility, biodegradation, and neovascularization of human single-unit platelet-rich fibrin glue: an in vivo analysis显示文摘 | Wu Xiuwen Ren Jianan Yao Genhong Zhou Bo Wang Gefei Gu Guosheng Luan Jianfeng | 2014 | Chinese Medical Journal2014，，3： | 3 |
| 14 | Type III interferon-induced CBFβinhibits HBV replication by hijacking HBx显示文摘Hepatitis B virus(HBV)and its associated chronic infection remain serious health threats worldwide.However,there is still no impactful approach for clinical treatment of hepatitis B patients.Therefore,developing a better understanding of the interactions between HBV and its host is particularly important.HBV infection has been reported to induce type-III but not type-I or type-II interferon(IFN).In this study,we identified CBFβ,an HIV enhancer,as an HBV restriction factor that is specifically induced by type-III IFN in the early stages of HBV infection.Type-III IFN-induced IL-10 played an important role in the production of CBFβ.Interestingly,the interaction between CBFβ-and HBV-encoded regulatory protein X(HBx)enhanced the stability of CBFβ,but notably blocked HBx-mediated promotion of HBV replication.CBFβexpression was lower in HBV patients than in healthy persons,and the addition of serum from HBV patients inhibited CBFβexpression in HepG2 cells.On the contrary,HBV via HBsAg inhibited type-III IFN-induced CBFβexpression and decreased the anti-HBV activity of type-III IFN,suggesting that HBV inhibits antiviral interferon-stimulated gene(ISG)expression and induces IFN resistance.Collectively,our results demonstrate that type-III IFN-triggered and IL-10-induced CBFβare crucial factors for inhibiting HBV replication,and the HBx–CBFβ–HBsAg axis reveals a new molecular mechanism of interaction between HBV and its hosts. | Fengchao Xu Hongxiao Song Qingfei Xiao Na Li Hong Zhang Genhong Cheng Guangyun Tan | 2019 | Cellular & Molecular Immunology2019，16，4： | 3 |
| 15 | 25-Hydroxycholesterol is a potent SARS-CoV-2 inhibitor显示文摘Dear Editor,As of July,2020,the ongoing pandemic of coronavirus diseases 2019(COVID-19)caused by the severe acute respiratory syndrome coronavirus 2(SARS-CoV-2,previously 2019-nCoV)has caused more than 10.3 million human infections,with more than 506,000 deaths worldwide according to the World Health Organization.The clinical manifestations of COVID-19 vary from no asymptomatic infection,mild“flu-like”symptoms,to lethal acute respiratory distress syndrome.The case mortality and fatality rates in people infected with SARS-CoV-2 increase steeply with age,and fatal outcomes are almost exclusively seen in people older than 50 years.1 Although the Food and Drug Administration has authorized emergency use of remdesivir for COVID-19 treatment in the US,the need for safe and effective antiviral drugs against SARS-CoV-2 remains urgent and unmet. | Shulong Zu Yong-Qiang Deng Chao Zhou Jie Li Lili Li Qi Chen Xiao-Feng Li Hui Zhao Sarah Gold Jun He Xiang Li Changqing Zhang Heng Yang Genhong Cheng Cheng-Feng Qin | 2020 | Cell Research2020，30，11： | 3 |
| 16 | The signaling adaptors and pathways activated by TNF superfamily显示文摘 | Paul W Dempsey Sean E Doyle Jeannie Q He Genhong Cheng | 2003 | Cytokine and Growth Factor Reviews2003，，3： | 2 |
| 17 | “Harmonious World”: Great Innovation Guiding the Development of China's Diplomatic Practice显示文摘Since the Sixteenth National Congress of the Communist Party of China, President Hu Jintao has elaborated on the strategic thought ofa | Kong Genhong Shi Dongmei | 2007 | International Understanding2007，，3： | 2 |
| 18 | A MyD88-dependent IFNyR-CCR2 signaling circuit is required for mobilization of monocytes and host defense against systemic bacterial challenge显示文摘 | Eric M Pietras Lloyd S Miller Carl T Johnson Ryan M O'Connell Paul W Dempsey Genhong Cheng | 2011 | Cell Research2011，21，7： | 2 |
| 19 | Clinicopathological fea- tures of the triple - negative tumors in Chinese breast cancer patients 显示文摘 | Yin Wenjin Lu Jinsong Di Genhong | 2009 | Breast Cancer Research and Treatment2009，115，2： | 1 |
| 20 | DDX1, DDX21, and DHX36 Helicases Form a Complex with the Adaptor Molecule TRIF to Sense dsRNA in Dendritic Cells显示文摘 | Zhiqiang Zhang Taeil Kim Musheng Bao Valeria Facchinetti Sung Yun Jung Amir Ali Ghaffari Jun Qin Genhong Cheng Yong-Jun Liu | 2011 | Immunity2011，，6： | 1 |
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