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| 1 | Construction and Identification of a Human Liver Specific MicroRNA Eukaryotic Expression Vector显示文摘MiR-122 is one of the non-coding RNAs which showed its effects on the lipo-metablism,virus infection and HCC forming through regulation of liver gene expression.Its eukaryotic expression vector was constructed by using pSuper which was widely applied in the siRNA expression.The precursor of human miR-122 gene was amplified by polymerase chain reaction(PCR)from the human genomic DNA.The positive clones were screened by PCR and restriction enzyme digestion.The new expression vector of miR-122 was named pHsa-m122.PHsa-m122 and its controls were transfected to HepG2 cells.The miR-122 expression activity was evaluated by GFP122i sensor reporter plasmid through fluorescence detection and Western blot.It was shown that the fluorescence intensity of GFP122si and pHsa-m122 co-transfection group was weaker than that of the controls,so the functional activity of expressed miR-122 was detected.When HepG2 cells were co-transfected with HBV1.3 and pHsa-m122 plasmids, the results showed miR-122 may down-regulate the gene expression of HBV.The human liver specific microRNA eukaryotic expression vector of miR-122 was constructed successfully,which may facilitate further study of its function in the development of liver virus infection diseases and HCC. | Shanshan Chen Ming Ni Bing Yu Tingting Lv Mengji Lu Feili Gong | 2007 | Cellular & Molecular Immunology2007，4，6： | 18 |
| 2 | IL-10 Gene Modified Dendritic Cells Inhibit T Helper Type 1-Mediated Alloimmune Responses and Promote Immunological Tolerance in Diabetes显示文摘Dendritic cells (DCs) have the potency to regulate the outcome of autoimmunity through the modulation of immune responses. The induction of antigen specific tolerance is critical for prevention and treatment of allograft rejection. In the present study,we transfected IL-10 gene into DCs and investigated their effect on inhibition of lymphocyte activity in vitro and induction of immune tolerance on islet allograft in mice. An IDDM C57BL/6 mouse model was induced by streptozotocin. The islet cells isolated from the BALB/c mice were transplanted into the kidney capules of the model mice followed by injection of IL-10 modified DCs (mDCs). The results showed that mDCs could significantly inhibit T lymphocyte proliferation mediated by allotype cells and induce its apoptosis,whereas,unmodified DCs (umDCs) could promote the murine lymphocyte proliferation markedly. The injection of mDCs could prolong the survival of allotype islet transplanted IDDM mice. The average plasma glucose (PG) level in mDCs treated mice returned to normal within 3 days and lasted for about 2 weeks. The rejection response in control mice occurred for 5 days after transplantation. The level of IFN-γ was lower while IL-4 was higher in mDCs treated mice than that in umDCs treated mice,which indicated that Th1/Th2 deviation occurred. Our studies suggest that IL-10 gene modified DCs can induce the immune tolerance to islet graft and prolong survival of the recipients by the inhibiting of T cell proliferation in allotype mice. | Huifen Zhu Wenhong Qiu Ping Lei Wei Zhou Xue Wen Fengrong He Li Li Hong Dai Guanxin Shen Feili Gong | 2008 | Cellular & Molecular Immunology2008，5，1： | 14 |
| 3 | Mutational Analysis of Region-cytotoxicity Relationship in Human Transmembrane Tumor Necrosis Factor-alpha显示文摘Objective:To determine the region of human transmembrane tumor necrosis factor-alpha (TM-TNFa), essential for cytotoxic activity a-gainst human breast cancer cell line MCF-7. Methods:Single amino-acid-substituted TM-TNFα mutant proteins (muteins) were produced by in vitro transcription linked translation techniques. The cDNA of TM-TNFα was site-directed mutagenized by recombinant PCR. Results:13 single amino-acid substituted TM-TNFα muteins were generated and assayed for cytotoxic activity. The cytotoxic activities of TM-TNFα muteins, eg, TM-TNFα-71/Lys, -28/Phe and 117/Leu were significantly decreased (P<0.01) compared to that of parent TM-TNFα, 143/Tyr decreased 4-folds, and-17/Thr,-39/Ser,ll9/His,35/Gly,95/Cys and 147/Phe decreased 1.5-2.5-folds, respectively. However, the cytotoxic activities of TM-TNFα-8/Arg, 31/Gly and 87/Phe showed no significant change. Conclusion:These results indicate that the regions associated with cytotoxic-activity of TM-TNFα are different with that of secretory TNF-lpha (S-TNFα). The inner cell region and transmembrane region of TM-TNFα are related to the cytotoxic activity of TM-TNFα. | ZHENG Fang, GONG Feili, LI Zhuoya, JIANG Xiaodan, XIONG Ping, FENG Wei, XU Yong, Institute of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China | 2002 | The Chinese-German Journal of Clinical Oncology2002，1，1： | 14 |
| 4 | Soluble Mouse B7-H3 Down-Regulates Dendritic Cell Stimulatory Capacity to Allogenic T Cell Proliferation and Production of IL-2 and IFN-γ显示文摘B7-H3 是 B7 基因家庭的一个最近识别的成员。它的无所不在的表示在淋巴并且 nonlymphoid 纸巾建议它能在自我忍耐的维护起一个重要作用。然而, B7-H3 的准确功能仍然是逃犯的。当前的学习的目的是为调停 DC 的 T 房间激活的预防表明可溶的老鼠 B7-H3 的可能的功能。为这个目的,我们建立了可溶的老鼠 B7-H3 熔化蛋白质(mB7h3-hIg ) 有 C 终端人的 IgG1 Fc 的真核细胞的表示向量(pmB7h3-hIg ) 。C57BL/6 (B6 ) 导出树枝状的房间线(DC2.4 房间) 为可溶的 mB7h3-hIg 的产生被用于稳定的 transfectants 的建立。宫外的 mB7h3-hIg 表示被 RT-PCR,西方的污点和 ELISA 分析证实。49.7 kD 蛋白质被西方的污点与 pmB7h3-hIg 从 DC2.4 房间 transfected 检测。可溶的 mB7h3-hIg 表示没在房间骑车和 apoptosis 和 CD80 的表示和 DC2.4 房间的 CD86 上有效果,这被发现。然而,宫外的可溶的 mB7h3-hIg 表示被发现显著地为 DC2.4 房间影响 allo-stimulatory 能力。当与 MLC.Further 决定的控制相比研究表明可溶的 mB7h3-hIg 能也禁止 IL-2 和建议的 allogenic T cells.These 结果的 IFN- 生产,表示可溶的 mB7h3-hIg 的 DC2.4 房间显示出一个重要减少的 allo-stimulatory 能力为接枝拒绝和 autoimmume 疾病的治疗的可溶的 B7-H3 的一个大潜力。 | Junfa Xu Baojun Huang Ping Xiong Wei Feng Yong Xu Min Fang Fang Zheng Feili Gong | 2006 | Cellular & Molecular Immunology2006，3，3： | 8 |
| 5 | Gene Delivery of SOCS3 Protects Mice from Lethal Endotoxic Shock显示文摘Suppressor of cytokine signaling 3 (SOCS3) was reported as a feedback inhibitor of cytokine receptor signaling by inhibiting the JAK-STAT signal transduction pathway. We sought to test the anti-endotoxic septic shock effect of liposome mediated gene delivery of SOCS3 in a lethal endotoxic shock mouse model. BALB/c mice were injected intraperitoneally with 200 μg pcDNA3.1-SOCS3 cationic liposomes, while pcDNA3.1-IL-10 and empty vector as positive and negative control respectively. Forty-eight hours after gene delivery, mice were challenged with 4 μg of E. coli 0127:B8 LPS and 18 mg D-GalN administered i.p. 90 min later, serum TNF-α level was determined. Survival over the next 48 h was evaluated. Peritoneal macrophages from survival mice were stimulated in vitro with 1 μg/ml LPS for 18 h, and the supernatants were harvested for determination of the amount of TNF-α. We found that gene delivery of SOCS3 significantly increase the mouse survival rate from 27.8 ± 9.6% of control group to 61.1 ± 9.6% (p < 0.01). In comparison with control group (218 ± 13 pg/ml) and sham delivery group (219 ± 22 pg/ml), gene delivery of SOCS3 reduced the level of serum TNF-α (68 ± 9 pg/ml) significantly (p < 0.01). Furthermore, gene delivery of SOCS3 displayed the capacity of prevention of tolerance of peritoneal macrophages to LPS. These findings suggest that gene delivery of SOCS3 mediated by liposome is a promising approach for endotoxic septic shock treatment. Cellular & Molecular Immunology. | Min Fang Hong Dai Guang Yu Feili Gong | 2005 | Cellular & Molecular Immunology2005，2，5： | 5 |
| 6 | KIR2DL2/C1 is a Risk Factor for Chronic Infection and Associated with Non-response to PEG-IFN and RBV Combination Therapy in Hepatitis C Virus Genotype 1b Patients in China显示文摘Dear Editor,Natural killer(NK)cells are lymphocytes that play important roles in the host defense against hepatitis C virus(HCV)infection.Killer cell immunoglobulin-like receptors(KIRs)are a group of regulatory molecules expressed on NK cells and a subset of T cells(Parham 2005).Ligands for KIRs are human leukocyte antigen(HLA)class Ⅰ molecules,and HLA-C1 is a ligand for the | Song Hu Fahu Yuan Lingyan Feng Fang Zheng Feili Gong Hanju Huang Binlian Sun | 2018 | Virologica Sinica2018，33，4： | 3 |
| 7 | Plasmacytoid dendritic cell deficiency in neonates enhances allergic airway inflammation via reduced production of IFN-α显示文摘Allergic asthma,a chronic inflammatory airway disease associated with type 2 cytokines,often originates in early life.Immune responses at an early age exhibit a Th2 cell bias,but the precise mechanisms remain elusive.Plasmacytoid dendritic cells(pDCs),which play a regulatory role in allergic asthma,were shown to be deficient in neonatal mice.We report here that this pDC deficiency renders neonatal mice more susceptible to severe allergic airway inflammation than adult mice in an OVA-induced experimental asthma model.Adoptive transfer of pDCs or administration of IFN-αto neonatal mice prevented the development of allergic inflammation in wild type but not in IFNAR1−/−mice.Similarly,adult mice developed more severe allergic inflammation when pDCs were depleted.The protective effects of pDCs were mediated by the pDC-/IFN-α-mediated negative regulation of the secretion of epithelial cell-derived CCL20,GM-CSF,and IL-33,which in turn impaired the recruitment of cDC2 and ILC2 cells to the airway.In asthmatic patients,the percentage of pDCs and the level of IFN-αwere lower in children than in adults.These results indicate that impairment of pDC-epithelial cell crosstalk in neonates is a susceptibility factor for the development of allergeninduced allergic airway inflammation. | Min Wu Liuchuang Gao Miao He Hangyu Liu Han Jiang Ketai Shi Runshi Shang Bing Liu Shan Gao Hebin Chen Feili Gong Erwin WGelfand Yafei Huang Junyan Han | 2020 | Cellular & Molecular Immunology2020，17，5： | 3 |
| 8 | HMGB1 from Astrocytes Promotes EAE by Influencing the Immune Cell Infiltration-Associated Functions of BMECs in Mice显示文摘High mobility group box 1(HMGB1)has been reported to play an important role in experimental autoimmune encephalomyelitis(EAE).Astrocytes are important components of neurovascular units and tightly appose the endothelial cells of microvessels by their perivascular endfeet and directly regulate the functions of the blood-brain barrier.Astrocytes express more HMGB1 during EAE while the exact roles of astrocytic HMGB1 in EAE have not been well elucidated.Here,using conditional-knockout mice,we found that astrocytic HMGB1 depletion decreased morbidity,delayed the onset time,and reduced the disease score and demyelination of EAE.Meanwhile,there were fewer immune cells,especially pathogenic T cells infiltration in the central nervous system of astrocytic HMGB1 conditional-knockout EAE mice,accompanied by up-regulated expression of the tight-junction protein Claudin5 and down-regulated expression of the cell adhesion molecules ICAM1 and VCAM1 in vivo.In vitro,HMGB1 released from astrocytes decreased Claudin5 while increased ICAM1 and VCAM1 expressed by brain microvascular endothelial cells(BMECs)through TLR4 or RAGE.Taken together,our results demonstrate that HMGB1 derived from astrocytes aggravates EAE by directly influencing the immune cell infiltration-associated functions of BMECs. | Junyu Shi Yifan Xiao Na Zhang Mengya Jiao Xuhuan Tang Chan Dai Chenchen Wang Yong Xu Zheng Tan Feili Gong Fang Zheng | 2022 | Neuroscience Bulletin2022，38，11： | 3 |
| 9 | Peptide-specific,allogeneic T cell response in vitro induced by a self-peptide binding to HLA-A2显示文摘The role of the bound peptide in alloreactive T-cell recognition is controversial, ranging from pep-tide-independent to peptide-specific recognition of alloreactive T-cells. The aim of this study is to find the evidence that there exist peptide/MHC complex (pMHC)-specific CTLs among alloreactive T cells generated with long-term mixed lymphocytes culture (LTMLC). A single pMHC was manipulated by loading the TAP-defective, HLA-A2 expressing T2 cells with a viral peptide (LMP2A426-434) or a self-peptide (Tyr369-377). The PBLs samples from 4 HLA-A2 positive (HLA-A2+ve) and 4 HLA-A2 negative (HLA-A2-ve) donors were included in this study. The HLA-A2+ve PBL co-cultured with the LMP2A426-434 pulsed T2 (T2/LMP) stands for the nominal T-cell response to a viral antigen, and the HLA-A2-ve PBLs co-cultured with the Tyr369-377 pulsed T2 (T2/Tyr) for alloreactive T-cell response to an allogeneic antigen. The specificity of the expanded CTLs after the LTMLC was detected by their specific cytotoxicity and binding ability to specific pMHC-tetramer. An HLA-A2 restricted, HIV peptide (Gag77-85)was included for control. The cultural bulk of HLA-A2+ve PBLs with the T2/LMP showed an elevated specific cytotoxicity against the T2/LMP compared to that against the T2/HIV (26.52%±3.72% vs 7.01%±0.87%, P<0.001), and an increased frequency of binding to LMP-tetramer compared to that binding to HIV-tetramer (0.98%±0.33% vs 0.05%±0.01%, P=0.0014). The cultural bulk of HLA-A2-ve PBLs with the T2/Tyr showed a more active cytotoxicity against the T2/Tyr than that against T2/HIV (28.07%±2.58% vs 6.87%±0.01 %, P<0.001), and a higher frequency of binding to the Tyr-tetramer than that binding to the HIV-tetramer (0.88%±0.3% vs 0.06%±0.03%, P=0.0018). Our results indicate that the LTMLC is able to expand the viral antigen-specific CTLs as well as allogeneic antigen-specific CTLs. A relatively large proportion of alloreactive CTLs should be pMHC-specific, i.e., the specificity of the alloreactive lines depends on both the bound peptide and the allotype of MHC. Our observations support the hypothesis that the cumulative effect of T cells specific to each peptide epitope could account for the strength and diversity of the alloresponse. The method using manipulated pMHC and the LTMLC to generate pMHC-specific, alloreactive CTLs is of potential importance for adoptive T-cell immunotherapy. | WENG XiuFang, LIANG ZhiHui, LU XiaoLing, ZHONG MaoHua, LU ShengJun, ZHANG CaiE, DENG Jing, WU XiongWen & GONG FeiLi Department of Immunology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China | 2007 | Science China(Life Sciences)2007，50，2： | 2 |
| 10 | Indoleamine 2,3-dioxygenase and regulatory dendritic cells contribute to the allograft protection induced by infusion of donor-specific splenic stromal cells显示文摘It has been reported that splenic stromal cells(SSCs)are capable of directly supporting the development of CD11c ^(lo)CD45RB^(+) IL-10-producing dendritic cells(DCs)from lineage-negative c-kit^(+) progenitor cells in the absence of exogenous cytokines.In vitro,DCs that differentiate on stromal cells suppress mixed leukocyte reaction responses and induce primary alloreactive CD4^(+) T cells to differentiate into IL-10-producing Tr1 cells.However,the precise mechanisms by which these SSCs exert their regulatory functions in vivo remain undefined.Furthermore,their possible contribution to the development of allograft transplantation tolerance has yet to be examined.Here,we have used both murine skin and cardiac allograft transplantation models to explore whether in vivo alloresponses can be regulated by infusion with donor-derived SSCs and to investigate the possible mechanisms by which SSCs exert regulatory effects to prevent allograft rejection.We show that intravenous SSC infusion prolonged murine skin allograft survival.The prolonged graft survival is associated with augmentation of the generation of regulatory DC subsets and CD4^(+) CD25^(+) Foxp3^(+) regulatory T cells(Tregs),as well as upregulation of the production of suppressive cytokines IL-10 and transforming growth factor(TGF)-b.Moreover,we found that indoleamine 2,3-dioxygenase and SSC-derived regulatory DCs contribute to allograft protection by infusion of donor-specific SSCs.Our data suggest that donor-derived SSCs could be used as a therapeutic target to promote transplantation tolerance. | Li Liu Lihua Duan Min Gong Hong Dai Quan Gong Fang Zheng Zheng Tan Congyi Wang Feili Gong Min Fang | 2011 | Cellular & Molecular Immunology2011，8，1： | 2 |
| 11 | ATP6V0d2 mediates leucine-induced mTORCI activation and polarization of macrophages显示文摘Dear Editor, mTORCI, as a center regulatory hub of metabolism, senses the cellular energy status, nutrition and extracellular stimuli and regulates cell growth, differentiation and functions of immune cells (Powell et al., 2012). Lysosomal localization of key signal comp orients is critical for mTORCI activati on: mTORCI activation requires co-localization of activated Rheb and mTORCI to the lysosome membrane (Buerger et al., 2006). Signals in eluding growth factors, cellular stresses and energy levels act on the disruption the formation of tuberous sclerosis complex (TSC) complex, comprised of TSC1, TSC2 and TBC1D7, which leads to the translocation and activation of Rheb on the lysosome membrane (Dibble et al., 2012). In response to nutrient levels, specifically the availability of amino acids and glucose (Efeyan et al., 2013), mTORCI is recruited to the lysosomal surface by Rag GTPases that are heterodimers of RagA or RagC bound to RagB or RagD. Multiple protein complexes have been implicated in regulation of mTORCI upon nutrient sensing including Ragulator, GATOR1, GATOR2, KICSTOR and vacuolar ATPases (Wolfson et al., 2017). Vacuolar ATPases are large multiple-protein complexes that acidify the lysosome and may mediate additional functions independent of their proton pump activity (Nishi and Forgac, 2002). | Pingfei Li Xiaofei Deng Jing Luo Yufei Chen Guoyu Bi Feili Gong Zhengping Wei Na Liu Huabin Li Arian Laurence Xiang-Ping Yang | 2019 | Protein & Cell2019，10，8： | 1 |
| 12 | Antitumor Effects of the Fibroblasts Transfected TNF-α Gene and its Mutants显示文摘Summary: To compare the anti-tumor effects of transmembrane TNF-α (TM-TNF) and secreted TNF-α (S-TNF) in vivo, mouse fibroblasts NIH3T3 were transfected separately with three types of retrovirus containing wild type TNF-α (Wt-TNF), TM-TNF mutant (TM-TNFm), S-TNF mutant (S-TNFm). Southern blot, RT-PCR, FACS and bioassay were used to investigate TNF-α gene integration, expression and its biological activity. It was found that both fixed cells and supernatant of NIH3T3/Wt-TNF, the fixed cells of NIH3T3/TM-TNFm and the supernatant of NIH3T3/S-TNFm could express high level of TNF-α or its mutants and effectively kill H22 in vitro. The transfected NIH3T3 were separately injected into the mice at the sites of H22 tumor cell inoculation according to a ratio of 5∶1 or 1∶1 (effector/target cells, E/T) after the third day of H22 challenge, respectively. At the E/T=5∶1, the NIH3T3/TM-TNFm induced the highest tumor regression, while NIH3T3/S-TNFm exerted the strongest tumor depressing effect at the E/T=1∶1 in vivo. No obvious side effects were noted throughout the course of treatment. The results suggest that both TM-TNF and S-TNF could cause tumor regression. The anti-tumor effect of TM-TNF would be more powerful and safe than that of S-TNF at the proper E/T ratio. | LI Qingfen(李清芬) LI Li (李莉) LI Zhuoya(李卓娅) GONG Feili(龚非力) FENG Wei(冯玮) JIANG Xiaodan(姜晓丹) XIONG Ping(熊平) | 2002 | Journal of Huazhong University of Science and Technology(Medical Sciences)2002，22，2： | 0 |
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