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  • Cell Research
    141 147 Anti viral innate immunity pathways Rashu B Seth 1 Lijun Sun 1 Zhijian J Chen 1 1 Howard Hughes Medical Institute Department of Molecular Biology University of Texas Southwestern Medical Center Dallas TX 75390 9148 USA Correspondence Zhijian J Chen Tel 214 648 1145 E mail Zhijian Chen UTSouthwestern edu Recent studies have uncovered two signaling pathways that activate the host innate immunity against viral infection One of the pathways utilizes members of the Toll like receptor TLR family to detect viruses that enter the endosome through endocytosis The TLR pathway induces interferon production through several signaling proteins that ultimately lead to the activation of the transcription factors NF κB IRF3 and IRF7 The other antiviral pathway uses the RNA helicase RIG I as the receptor for intracellular viral double stranded RNA RIG I activates NF κB and IRFs through the recently identified adaptor protein MAVS a CARD domain containing protein that resides in the mitochondrial membrane MAVS is essential for antiviral innate immunity but it also serves as a target of Hepatitis C virus HCV which employs a viral protease to cleave MAVS off the mitochondria thereby allowing HCV to escape the host immune system Cell Research

    Original URL path: http://www.cell-research.com/arts.asp?id=1103 (2016-02-14)
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  • Cell Research
    91120 Jerusalem Israel Correspondence Raymond Kaempfer Tel 972 2 675 8389 E mail kaempfer hebrew edu PKR the interferon IFN inducible protein kinase activated by double stranded RNA inhibits translation by phosphorylating the initiation factor eIF2a chain Uniquely human IFN γ mRNA uses local activation of PKR in the cell to control its own translation yield IFN γ mRNA activates PKR through a structure in its 5 region harboring a pseudoknot which is critical for PKR activation Mutations that impair pseudoknot stability reduce the ability of IFN γ mRNA to activate PKR and strongly increase its translation efficiency The cis acting RNA element in IFN γ mRNA functions as a biological sensor of intracellular PKR levels During an immune response as IFN γ and other inflammatory cytokines build up in the cell s microenvironment they act to induce higher levels of PKR in the cell resulting in a more extensive activation of PKR by IFN γ mRNA With the resulting phosphorylation of eIF2a a negative feedback loop is created and the production of IFN γ is progressively attenuated We propose that the therapeutic effect of IFN β in multiple sclerosis may rest at least in part on its exquisite ability

    Original URL path: http://www.cell-research.com/arts.asp?id=1104 (2016-02-14)
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  • Cell Research
    Loss of self tolerance and expansion of auto reactive lymphocytes are the basis for autoimmunity Apoptosis and the rapid clearance of apoptotic cells by phagocytes usually occur as coordinated processes that ensure regulated cellularity and stress response with non pathological outcomes Defects in clearance of apoptotic cells would contribute to the generation of self reactive lymphocytes which drive autoimmune disorders such as rheumatoid arthritis RA and systemic lupus erythematosus SLE The IL 12 family of cytokines IL 12 IL 23 and IL 27 and IL 10 are produced by phagocytic macrophages and play critical roles in the regulation of antigen presenting cells APCs and effector lymphocytes during an immune response to pathogens Inappropriate expression of these cytokines and their dysregulated activities have been strongly implicated in the pathogenesis of several autoimmune diseases The production of pro and anti inflammatory cytokines by phagocytic APCs is delicately regulated during the ingestion of apoptotic cells as part of an intrinsic mechanism to prevent inflammatory autoimmune reactions How apoptotic cell derived signals regulate cytokine production is poorly understood A recent study by our group demonstrated that phagocytosis of apoptotic cells by activated macrophages results in strong inhibition of IL 12 p35 gene expression by

    Original URL path: http://www.cell-research.com/arts.asp?id=1105 (2016-02-14)
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  • Cell Research
    Xu 1 Ban Hock Toh 1 Jun Ping Liu 1 1 Department of Immunology Molecular Signaling Laboratory Monash University Melbourne Australia Correspondence He Li Tel 61 3 99030715 E mail he li med monash edu au Transforming growth factor β TGF β carries out tumor suppressor activity in epithelial and lymphoid cells whereas telomerase is required for most cancers Although the molecular mechanisms by which TGF β acts as a tumor suppressor are yet to be fully established a link between TGFb and its tumor suppressor activity by telomerase has been suggested Recently we have noted a novel mode of action for TGF β through which human telomerase reverse transcriptase hTERT gene is repressed in immortal and neoplastic cells confirming that one of the mechanisms underlying TGF β suppression of tumor growth may be through inhibiting hTERT gene transcription Moreover the inhibition of hTERT gene by TGF β suggests a cis action of the TGF β signaling molecule Smad3 on hTERT promoter directly This article examines our current understanding and investigation of TGF β regulation of telomerase activity and presents a model in which Smad3 participates in regulating hTERT gene transcription by acting as a repressor directly Engineering the interface

    Original URL path: http://www.cell-research.com/arts.asp?id=1107 (2016-02-14)
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  • Cell Research
    and paracrine manner by blocking the attachment of HIV particles to permissive cells MK mRNA is systematically expressed in adult peripheral blood lymphocytes from healthy donors while its expression becomes markedly but transiently increased upon in vitro treatment of lymphocytes with IL 2 or IFN g and activation of T lymphocytes by PHA or through the engagement of the CD28 antigen The binding of MK to cells occurs specifically at a high and a low affinity binding site This low affinity binding site is the cell surface expressed nucleolin which is implicated in the mechanism of the initial attachment of HIV particles to cells Accordingly the nucleolin binding HB 19 pseudopeptide has no effect on the MK binding to the high affinity binding site whereas it prevents the binding of MK to the low affinity binding site thus suggesting the low affinity receptor of MK is the cell surface expressed nucleolin Confocal immunofluorescence laser microscopy revealed the colocalization of MK and the cell surface expressed nucleolin at distinct spots The use of various deletion constructs of nucleolin then indicates that the extreme C terminal end of nucleolin containing repeats of the amino acid motif RGG as the domain that binds

    Original URL path: http://www.cell-research.com/arts.asp?id=1108 (2016-02-14)
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  • Cell Research
    Sciences Zhejiang Sci Tech University Hangzhou China 2 Institute of Biochemistry and Cell Biology Chinese Academy of Sciences Shanghai 200031 China 3 Division of Gene Therapy and Hepatology CIMA University of Navarra Pamplona 31008 Spain Correspondence Cheng Qian Tel 34 948 194700 E mail cqian unav es Gene therapy offers a new approach for treatment of cancer Transfer of genes encoding immunostimulatory cytokines has been used with remarkable success to eliminate cancer in animals However clinical trials in patients with this strategy had limited efficacy Therefore improvement of gene transfer vector system is necessary A hybrid viral vector consisting of SFV replicon with either murine IL 12 or reporter LacZ gene was constructed This hybrid vector showed specificity and high level of expression in HCC both in vitro and in vivo In a rat orthotropic liver tumor model treatment of established tumors by the hybrid vector with mIL 12 gene resulted in a strong anti tumor activity without accompanying toxicity Subsequently a helper dependent adenovirus vectors containing a mifepristone RU486 inducible system was constructed for controlled and liver specific expression of human interleukin 12 hIL 12 HD Ad RUhIL 12 and mouse IL 12 mIL 12 HD Ad RUmIL 12 Data showed that high and sustained serum levels of hIL 12 could be attained by continuing administration of RU486 every 12 or 24 h Repetitive induction of hIL 12 could be obtained over at least a period of 48 weeks after a single injection of HD Ad RUhIL 12 Treatment of liver metastases with of HD Ad RUmIL 12 plus RU846 resulted in complete tumor regression in all animals Then different cytokine genes were inserted into conditional replicative adenoviruses vectors also called oncolytic adenovirus Replication of adenovirus in tumor cells would kill tumor cells and release viruses which infect surrounding

    Original URL path: http://www.cell-research.com/arts.asp?id=1109 (2016-02-14)
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  • Cell Research
    for Veterinary Biotechnology Shanghai Jiao Tong University Shanghai 200030 China 3 Xinyuan Institute of Medicine and Biotechnology School of Life Sciences Zhejiang University of Technology and Sciences Hangzhou 310018 China Correspondence Wei Han Tel 86 21 34202750 E mail weihan sjtu edu cn The cellular basis of bone marrow BM tissue development and regeneration is mediated through hematopoietic stem cells HSCs and mesenchymal stem cells MSCs Local interplays between hematopoietic cells and BM stromal cells BMSCs determine the reconstitution of hematopoiesis after myelosuppression Here we review the BM local signals in control of BM regeneration after insults Hematopoietic growth factors HGFs and cytokines produced by BMSCs are primary factors in regulation of BM hematopoiesis Morphogens which are critical to early embryo development in multiple species have been added to the family of HSCs regulators including families of Wnt proteins Notch ligands BMPs and Hedgehogs Global gene expression analysis of HSCs and BMSCs has begun to reveal signature groups of genes for both cell types More importantly analysis of global gene expression coupled with biochemical and biological studies of local signals during BM regeneration have strongly suggested that HGFs and cytokines may not be the primary local regulators for BM recovery

    Original URL path: http://www.cell-research.com/arts.asp?id=1110 (2016-02-14)
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  • Cell Research
    mednet ucla edu Cytokines activate multiple signal transduction pathways to regulate gene expression STATs and NF kB are two important families of transcription factors activated by cytokines Abnormal regulation of STAT and NF kB activities has been associated with human diseases The protein inhibitor of activated STAT PIAS protein family has been proposed to interact with over 60 proteins many of which are transcription factors involved in the immune system

    Original URL path: http://www.cell-research.com/arts.asp?id=1111 (2016-02-14)
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