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Journal of autoimmunity 14건

  1. [해외논문]   Editorial Board   SCI SCIE


    Journal of autoimmunity v.85 ,pp. i - i , 2017 , 0896-8411 ,

    초록

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  2. [해외논문]   Wandering pathways in the regulation of innate immunity and inflammation   SCI SCIE

    Mantovani, Alberto (Humanitas Clinical and Research Center, Via Manzoni 56, 20089, Rozzano, Milan, Italy)
    Journal of autoimmunity v.85 ,pp. 1 - 5 , 2017 , 0896-8411 ,

    초록

    Abstract Tumor-associated macrophages (TAM) have served as a paradigm of cancer-related inflammation. Moreover, investigations on TAM have led to the dissection of macrophage plasticity and polarization and to the discovery and analysis of molecular pathways of innate immunity, in particular cytokines, chemokines and PTX3 as a prototypic fluid phase pattern recognition molecule. Mechanisms of negative regulation are complex and include decoy receptors, receptor antagonists, anti-inflammatory cytokines and the signalling regulator IL-1R8. In this review, topics and open issues in relation to regulation of innate immunity and inflammation are discussed: 1) how macrophage and neutrophil plasticity and polarization underlie diverse pathological conditions ranging from autoimmunity to cancer and may pave the way to innovative diagnostic and therapeutic approaches; 2) the key role of decoy receptors and negative regulators (e.g. IL-1R2, ACKR2, IL-1R8) in striking a balance between amplification of immunity and resolution versus uncontrolled inflammation and tissue damage; 3) role of humoral innate immunity, illustrated by PTX3, in resistance against selected microbes, regulation of inflammation and immunity and tissue repair, with implications for diagnostic and therapeutic translation. Highlights Macrophage plasticity and polarization is a fundamental mechanism involved in inflammation, autoimmunity and cancer. Decoy receptors are an evolutionary conserved mechanism to regulate the action of cytokines and chemokines. Negative regulators are key to balance amplification of immunity and uncontrolled inflammation and tissue damage. Negative regulators are essential for resolution of inflammation, whose failure determines immunopathology.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  3. [해외논문]   Direct targeting of cancer cells with antibodies: What can we learn from the successes and failure of unconjugated antibodies for lymphoid neoplasias?   SCI SCIE

    Golay, José , e
    Journal of autoimmunity v.85 ,pp. 6 - 19 , 2017 , 0896-8411 ,

    초록

    Abstract Following approval in 1997 of the anti-CD20 antibody rituximab for the treatment of B-NHL and CLL, many other unconjugated IgG1 MAbs have been tested in pre-clinical and clinical trials for the treatment of lymphoid neoplasms. Relatively few have been approved however and these are directed against a limited number of target antigens (CD20, CD52, CCR4, CD38, CD319). We review here the known biological properties of these antibodies and discuss which factors may have led to their success or may, on the contrary, limit their clinical application. Common factors of the approved MAbs are that the target antigen is expressed at relatively high levels on the neoplastic targets and their mechanism of action is mostly immune-mediated. Indeed most of these MAbs induce ADCC and phagocytosis by macrophages, and many also activate complement, leading to target cell lysis. In contrast direct cell death induction is not a common feature but may enhance efficacy in some cases. Interestingly, a key factor for the success of several MAbs appears to be their capacity to skew immunity towards an anti-tumour mode, by inhibiting/depleting suppressor cells and/or activating immune cells within the microenvironment, independently of FcγRs. We also expose here some of the strategies employed by industry to expand the clinical use of these molecules beyond their original indication. Interestingly, due to the central role of lymphocytes in the control of the immune response, several of the antibodies are now successfully used to treat many different autoimmune diseases and have also been formally approved for some of these new indications. There is little doubt that this trend will continue and that the precise mechanisms of therapeutic MAbs will be further dissected and better understood in the context of both tumour immunology and autoimmunity. Highlights Relatively few naked IgG1 MAbs have been approved for the treatment of lymphoid tumours. These MAbs share the ability to activate the immune system, directly or indirectly. The strategies for MAb development include modified molecules and new targets. These MAbs have seen the extension of their indication to several autoimmune diseases. The combination of MAbs with small drugs and best regimen still need optimization.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  4. [해외논문]   Small molecules to the rescue: Inhibition of cytokine signaling in immune-mediated diseases   SCI SCIE

    Gadina, Massimo (Corresponding author. Translational Immunology Section, Office of Science and Technology, National Institute of Arthritis Musculoskeletal and Skin Diseases, National Institutes of Health, Building 10, Room 10C101-C, Bethesda, MD, 20892-1560, USA.) , Gazaniga, Nathalia , Vian, Laura , Furumoto, Yasuko
    Journal of autoimmunity v.85 ,pp. 20 - 31 , 2017 , 0896-8411 ,

    초록

    Abstract Cytokines are small, secreted proteins associated with the maintenance of immune homeostasis but also implicated with the pathogenesis of several autoimmune and inflammatory diseases. Biologic agents blocking cytokines or their receptors have revolutionized the treatment of such pathologies. Nonetheless, some patients fail to respond to these drugs or do not achieve complete remission. The signal transduction originating from membrane-bound cytokine receptors is an intricate network of events that lead to gene expression and ultimately regulate cellular functionality. Our understanding of the intracellular actions that molecules such as interleukins, interferons (IFNs) and tumor necrosis factor (TNF) set into motion has greatly increased in the past few years, making it possible to interfere with cytokines' signaling cascades. The Janus kinase (JAK)/signal transducer and activator of transcription (STAT), the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), the mitogen activated protein kinase (MAPK) and the Phosphatidylinositol-3′-kinases (PI3K) pathways have all been intensively studied and key steps as well as molecules have been identified. These research efforts have led to the development of a new generation of small molecule inhibitors. Drugs capable of blocking JAK enzymatic activity or interfering with the proteasome-mediated degradation of intermediates in the NF-kB pathway have already entered the clinical arena confirming the validity of this approach. In this review, we have recapitulated the biochemical events downstream of cytokine receptors and discussed some of the drugs which have already been successfully utilized in the clinic. Moreover, we have highlighted some of the new molecules that are currently being developed for the treatment of immune-mediated pathologies and malignancies. Highlights Cytokines regulates the immune response but are also implicated in the development of several immune mediated diseases. Blocking cytokines or their receptors has been successfully employed to treat patients. Targeting the signal downstream of cytokine receptors has now been employed to generate new and effective drugs.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  5. [해외논문]   CIK as therapeutic agents against tumors   SCI SCIE

    Introna, M. (Presidio Matteo Rota, via Garibaldi 11-13, 24124, Bergamo, Italy.)
    Journal of autoimmunity v.85 ,pp. 32 - 44 , 2017 , 0896-8411 ,

    초록

    Abstract Cytokine Induced Killer (CIK) cells are ex vivo expanded and activated T lymphocytes obtained by sequential incubation of Peripheral Blood Mononuclear cells (PBMNC) with Interferon γ (IFNG), anti CD3 monoclonal antibody OKT3 and IL2. These cells, while retaining few characteristics of the Effector memory T cells subpopulation, acquired during culture CD56 expression, as well as non specific, Natural Killer like, anti tumoral cytotoxicity. CIK cells from human are equivalent to expanded NKT cells in mouse. More interestingly, CIK cells show a potent intratumoral homing in several experimental models, followed by anti tumoral clinical activity in mice and humans. In spite of extensive in vivo permanence and proliferation, CIK cells do not show cytotoxicity against normal targets and, particularly important, do not show Graft versus host disease when tested in allogeneic combinations (donor versus host) even in the haploidentical matching. For the easiness of the laboratory preparations, the availability of clinical grade reagents, the production of Good Manufacturing Practice compliant methods, CIK cells have been extensively used for the treatment of cancer patients, in both hematologic and solid tumors, in both autologous and allogeneic combinations. Several clinical protocol will be here discussed and summarised to show the feasibility of these passive transfer approaches, and also their very limited toxicity. Finally, preliminary indications on clinical efficacy, particularly in hematologic malignancies and against minimal residual disease, will be shown and discussed, as well as the future perspectives to optimize this adoptive passive cell immunotherapy strategy by gene transfer technology or bispecific monoclonal antibodies addition. Highlights Cytokine Induced Killer (CIK) cells are T-EMRA CD8 + lymphocytes which express CD56. CIK cells show intratumoral homing and antitumoral activity. CIK cells can be used in autologous as well as allogeneic combination without toxicity. The standard protocol for CIK preparation is GMP compliant.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [해외논문]   Chemokine isoforms and processing in inflammation and immunity   SCI SCIE

    Proost, Paul (Laboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven, University of Leuven, Herestraat 49, B-3000, Leuven, Belgium ) , Struyf, Sofie (Laboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven, University of Leuven, Herestraat 49, B-3000, Leuven, Belgium ) , Van Damme, Jo (Laboratory of Molecular Immunology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven, University of Leuven, Herestraat 49, B-3000, Leuven, Belgium ) , Fiten, Pierre (Laboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven, University of Leuven, Herestraat 49, B-3000, Leuven, Belgium ) , Ugarte-Berzal, Estefania (Laboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven, University of Leuven, Herestraat 49, B-3000, Leuven, Belgium ) , Opdenakker, Ghislain (Laboratory of Immunobiology, Department of Microbiology and Immu)
    Journal of autoimmunity v.85 ,pp. 45 - 57 , 2017 , 0896-8411 ,

    초록

    Abstract The first dimension of chemokine heterogeneity is reflected by their discovery and purification as natural proteins. Each of those chemokines attracted a specific inflammatory leukocyte type. With the introduction of genomic technologies, a second wave of chemokine heterogeneity was established by the discovery of putative chemokine-like sequences and by demonstrating chemotactic activity of the gene products in physiological leukocyte homing. In the postgenomic era, the third dimension of chemokine heterogeneity is the description of posttranslational modifications on most chemokines. Proteolysis of chemokines, for instance by dipeptidyl peptidase IV (DPP IV/CD26) and by matrix metalloproteinases (MMPs) is already well established as a biological control mechanism to activate, potentiate, dampen or abrogate chemokine activities. Other posttranslational modifications are less known. Theoretical N-linked and O-linked attachment sites for chemokine glycosylation were searched with bio-informatic tools and it was found that most chemokines are not glycosylated. These findings are corroborated with a low number of experimental studies demonstrating N- or O-glycosylation of natural chemokine ligands. Because attached oligosaccharides protect proteins against proteolytic degradation, their absence may explain the fast turnover of chemokines in the protease-rich environments of infection and inflammation. All chemokines interact with G protein-coupled receptors (GPCRs) and glycosaminoglycans (GAGs). Whether lectin-like GAG-binding induces cellular signaling is not clear, but these interactions are important for leukocyte migration and have already been exploited to reduce inflammation. In addition to selective proteolysis, citrullination and nitration/nitrosylation are being added as biologically relevant modifications contributing to functional chemokine heterogeneity. Resulting chemokine isoforms with reduced affinity for GPCRs reduce leukocyte migration in various models of inflammation. Here, these third dimension modifications are compared, with reflections on the biological and pathological contexts in which these posttranslational modifications take place and contribute to the repertoire of chemokine functions and with an emphasis on autoimmune diseases. Highlights CD26 regulates leukocyte migration to arthritic joints through chemokine truncation. Chemokine cleavage by matrix metalloproteases affects autoimmunity. Chemokine glycosylation protects against proteolysis. Chemokines interact with glycosaminoglycans in inflammation. Peptidylarginine deiminases, active in autoimmune diseases, also citrullinate chemokines.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  7. [해외논문]   Inflammation and myeloproliferative neoplasms   SCI SCIE

    Lussana, Federico (Hematology and Bone Marrow Transplant Unit, ASST Papa Giovanni XXIII, Bergamo, Italy ) , Rambaldi, Alessandro (Hematology and Bone Marrow Transplant Unit, ASST Papa Giovanni XXIII, Bergamo, Italy)
    Journal of autoimmunity v.85 ,pp. 58 - 63 , 2017 , 0896-8411 ,

    초록

    Abstract Myeloproliferative neoplasms (MPN) include three main entities: Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Myelofibrosis (MF). MPN represent a unique model of the relationship between the clonal development of a hematologic malignancy and chronic inflammation. The neoplastic clone is the main driver of this inflammatory reaction as demonstrated by the curative effect of allogeneic stem cell transplantation which leads not only to a complete restore of the hematopoiesis, but also to regression of bone marrow fibrosis. The neoplastic clone and its differentiated progeny are also the main source of an indirect paracrine secretion of inflammatory cytokines released by different normal cells present within the tumor microenvironment. In the end, the cytokine storm within the bone marrow niche leads to fibrosis. In addition, chronic inflammation is responsible of the constitutional symptoms which negatively affect the quality of life of MPN patients and represents a major driver for the development of premature atherosclerosis and disease progression. Here we describe the available data about the link between MPN and chronic inflammation in animal models as well as in clinical studies. We also review the practical value of including acute phase inflammatory proteins such as high sensitivity C-reactive protein (hs-CRP) and pentraxin 3 (PTX-3) in prognostic stratification of MPN patients. Interestingly, the plasma levels of these proteins is often increase in MPN patients and this may be important when considering the well-established link between these two inflammatory proteins and the risk of both arterial and venous thrombosis. Although the available drugs are unable to eradicate the malignant clone, the ability to identify patient with a high inflammatory burden and an adverse molecular profile is important to advise therapy with ruxolitinib or even allogeneic stem cell transplantation that currently represents the only potentially curative option for these diseases. Highlights Chronic inflammation has been associated with myeloproliferative neoplasm (MPN). Different mediators of inflammation are increased in the serum of MPN patients. Some of the complications and symptoms can be linked to high inflammation burden. The prognostic value of acute phase inflammatory proteins in MPN has been evaluated. Treatment strategies should target the clonal hematopoiesis, key driver of inflammation.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  8. [해외논문]   Regulation of inflammation by members of the formyl-peptide receptor family   SCI SCIE

    Chen, Keqiang (Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA ) , Bao, Zhiyao (Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA ) , Gong, Wanghua (Basic Research Program, Leidos Biomedical Research, Inc., Frederick, MD, 21702, USA ) , Tang, Peng (Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA ) , Yoshimura, Teizo (Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8558, Japan ) , Wang, Ji Ming (Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702, USA)
    Journal of autoimmunity v.85 ,pp. 64 - 77 , 2017 , 0896-8411 ,

    초록

    Abstract Inflammation is associated with a variety of diseases. The hallmark of inflammation is leukocyte infiltration at disease sites in response to pathogen- or damage-associated chemotactic molecular patterns (PAMPs and MAMPs), which are recognized by a superfamily of seven transmembrane, Gi-protein-coupled receptors (GPCRs) on cell surface. Chemotactic GPCRs are composed of two major subfamilies: the classical GPCRs and chemokine GPCRs. Formyl-peptide receptors (FPRs) belong to the classical chemotactic GPCR subfamily with unique properties that are increasingly appreciated for their expression on diverse host cell types and the capacity to interact with a plethora of chemotactic PAMPs and MAMPs. Three FPRs have been identified in human: FPR1–FPR3, with putative corresponding mouse counterparts. FPR expression was initially described in myeloid cells but subsequently in many non-hematopoietic cells including cancer cells. Accumulating evidence demonstrates that FPRs possess multiple functions in addition to controlling inflammation, and participate in the processes of many pathophysiologic conditions. They are not only critical mediators of myeloid cell trafficking, but are also implicated in tissue repair, angiogenesis and protection against inflammation-associated tumorigenesis. A series recent discoveries have greatly expanded the scope of FPRs in host defense which uncovered the essential participation of FPRs in step-wise trafficking of myeloid cells including neutrophils and dendritic cells (DCs) in host responses to bacterial infection, tissue injury and wound healing. Also of great interest is the FPRs are exploited by malignant cancer cells for their growth, invasion and metastasis. In this article, we review the current understanding of FPRs concerning their expression in a vast array of cell types, their involvement in guiding leukocyte trafficking in pathophysiological conditions, and their capacity to promote the differentiation of immune cells, their participation in tumor-associated inflammation and cancer progression. The close association of FPRs with human diseases and cancer indicates their potential as targets for the development of therapeutics. Highlights FPRs have a multitude of agonists and are expressed by a great variety of cell types, including cancer cells. FPRs is important in controlling leukocyte trafficking and immune responses. FPRs also play an important role in inflammation associated tumorigenesis. Fpr2 deficiency impairs restoration of the colonic epithelial layer after injury. Many tumor cells express FPRs to stimulate tumor cell proliferation, metastasis and angiogenesis.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  9. [해외논문]   Modulation of inflammatory and immune responses by vitamin D   SCI SCIE

    Colotta, Francesco (DiaSorin SpA, Saluggia, VC, Italy ) , Jansson, Birger (DiaSorin SpA, Saluggia, VC, Italy ) , Bonelli, Fabrizio (DiaSorin Inc, Stillwater, MN, USA)
    Journal of autoimmunity v.85 ,pp. 78 - 97 , 2017 , 0896-8411 ,

    초록

    Abstract Vitamin D (VitD) is a prohormone most noted for the regulation of calcium and phosphate levels in circulation, and thus of bone metabolism. Inflammatory and immune cells not only convert inactive VitD metabolites into calcitriol, the active form of VitD, but also express the nuclear receptor of VitD that modulates differentiation, activation and proliferation of these cells. In vitro, calcitriol upregulates different anti-inflammatory pathways and downregulates molecules that activate immune and inflammatory cells. Administration of VitD has beneficial effects in a number of experimental models of autoimmune disease. Epidemiologic studies have indicated that VitD insufficiency is frequently associated with immune disorders and infectious diseases, exacerbated by increasing evidence of suboptimal VitD status in populations worldwide. To date, however, most interventional studies in human inflammatory and immune diseases with VitD supplementation have proven to be inconclusive. One of the reasons could be that the main VitD metabolite measured in these studies was the 25-hydroxyVitD (25OHD) rather than its active form calcitriol. Although our knowledge of calcitriol as modulator of immune and inflammatory reactions has dramatically increased in the past decades, further in vivo and clinical studies are needed to confirm the potential benefits of VitD in the control of immune and inflammatory conditions. Highlights VitD upregulates anti-inflammatory mediators and reduces inflammatory molecules in inflammatory and immune cells. Low levels of serum 25OHD correlate with autoimmune, inflammatory and infectious conditions in animal models and in humans. VitD administration has beneficial effects in different animal models of autoimmune diseases. VitD supplementation has generated inconclusive results in autoimmune and inflammatory diseases, requiring additional studies.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  10. [해외논문]   Twenty-five years of gene therapy for genetic diseases and leukemia: The road to marketing authorization of the first ex vivo gene therapies   SCI SCIE

    Bordignon, Claudio
    Journal of autoimmunity v.85 ,pp. 98 - 102 , 2017 , 0896-8411 ,

    초록

    Highlights Ex vivo gene therapy for genetic diseases and cancer. Genetic engineering of peripheral blood lymphocytes and hematopoietic stem cells. Complexities in the development of new therapeutics based on cell and gene manipulation.

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