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Clinical immunology : the official journal of the ... 49건

  1. [해외논문]   Ficolin-2 triggers antitumor effect by activating macrophages and CD8+ T cells   SCI SCIE SCOPUS

    Ding, Quanquan (State Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology and Department of Immunology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, PR China ) , Shen, Yanying (State Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology and Department of Immunology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, PR China ) , Li, Dongqing (Department of Microbiology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, PR China ) , Yang, Juan (State Key Laboratory of Virology and Medical Research Institute, Hubei Province Key Laboratory of Allergy and Immunology and Department of Immunology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, PR China ) , Yu, Jing (Hubei Province Cancer Hospital, Wuhan 430079, PR China ) , Yin, Zhinan (Biomedical Translational Research Institute, Jinan University, Guangzhou, Guangdong 510630, PR China ) , Zhang, Xiao-Lian (State Key Laboratory of Virology and Medical Research I)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 145 - 157 , 2017 , 1521-6616 ,

    초록

    Abstract Ficolin-2 is an important serum complement lectin. Here, we describe novel findings indicating that serum ficolin-2 concentrations in multiple tumor patients are significantly lower than those in healthy donors. Administration of exogenous ficolin-2 or ficolin-A (a ficolin-2-like molecule in mouse), with only once, could remarkably inhibit the tumor cells growth in murine tumor models via early macrophages, dendritic cells (DCs) and CD8 + T cells, but not CD4 + T cells. Ficolin-A (FCN-A) knockout (KO) mice exhibits significantly increased tumor cell growth. Ficolin-2 induces macrophage activation, promotes M1 polarization and facilitates proliferation and antigen-specific cytotoxicity of CD8 + T cells. Ficolin-2 binds to Toll-like receptor 4 (TLR4) on macrophages and DCs and promotes their antigen-presenting abilities to CD8 + T cells. Our findings provide a new therapeutic strategy for tumors based on the triggering of immune-mediated antitumor effect by ficolin-2. Highlights Ficolin-2/A inhibits tumor growth in vivo via early macrophages, DCs and CD8 + T cells. Binding of ficolin-2 with TLR4 induces macrophage activation and M1 polarization. Ficolin-2 enhances the proliferation of antigen-specific CD8 + T cells via binding and activating macrophages and DCs. Ficolin-2 induces macrophages to release TNF-α, IL-6, CCL5 and NO. Serum ficolin-2 levels in multiple tumor patients were much lower than those in healthy donors.

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  2. [해외논문]   Role of S100A9 in the development of neutrophilic inflammation in asthmatics and in a murine model   SCI SCIE SCOPUS

    Lee, Tae-Hyeong (Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Bucheon, Gyeonggi-do 420-767, Republic of Korea ) , Chang, Hun Soo (Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Bucheon, Gyeonggi-do 420-767, Republic of Korea ) , Bae, Da-Jeong (Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Bucheon, Gyeonggi-do 420-767, Republic of Korea ) , Song, Hyun Ji (Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Bucheon, Gyeonggi-do 420-767, Republic of Korea ) , Kim, Myung-Sin (Department of Internal Medicine, Soonchunhyang University Gumi Hospital, Gumi, Gyeongsangbuk-do 39371, Republic of Korea ) , Park, Jong Sook (Division of Allergy and Respiratory Disease, Soonchunhyang University Bucheon Hospital, 1174 Jung-dong, Bucheon, Gyeonggi-do 420-767, Republic of Korea ) , Jun, Ji Ae (Department of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Bucheon, Gyeonggi-do 42) , Lee, Si Young , Uh, Soo Taek , Kim, Soo Hyun , Park, Choon-Sik
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 158 - 166 , 2017 , 1521-6616 ,

    초록

    Abstract S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response. To investigate the role of S100A9 in neutrophilic asthma, S100A9 levels were measured in sputum from 101 steroid-naIve asthmatics using an ELISA kit and the levels were significantly correlated with percentages of neutrophils in sputum. Intranasal administration of recombinant S100A9 markedly increased neutrophil numbers at 8h and 24h later with concomitant elevation of IL-1β, IL-17, and IFN-γ levels. Treatment with an anti-S100A9 antibody restored the increased numbers of neutrophils and the increased airway resistance in OVA/CFA mice toward the levels of sham-treated mice. Concomitantly, the S100A9 and neutrophil elastase double positive cells were markedly reduced with attenuation of IL-1β, IL-17, and IFN-γ levels by the treatment with the anti-S100A9 antibody. Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation in asthma, possibly via inducing IL-1β, IL-17 and IFN-γ. Highlight S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response. Our data support a role of S100A9 to initiate and amplify the neutrophilic inflammation via inducing IL-1β, IL-17 and IFN-γ. Modulation of S100A9 in the airway may be a therapeutic strategy to control neutrophilic inflammation in asthma.

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  3. [해외논문]   Antibodies targeting BTLA or TIM-3 enhance HIV-1 specific T cell responses in combination with PD-1 blockade   SCI SCIE SCOPUS

    Grabmeier-Pfistershammer, Katharina (Division of Clinical and Experimental Immunology, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria ) , Stecher, Carmen (Division of Immune Receptors and T cell Activation, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria ) , Zettl, Markus (Cancer Immunology and Immune Modulation, Boehringer Ingelheim RCV GmbH & CoKG, Vienna, Austria ) , Rosskopf, Sandra (Division of Immune Receptors and T cell Activation, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria ) , Rieger, Armin (Department of Dermatology, Medical University of Vienna, Vienna, Austria ) , Zlabinger, Gerhard J. (Division of Clinical and Experimental Immunology, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria ) , Steinberger, Peter (Division of Immune Receptors and T cell Activation, Institute of Immunology, Center for Pathophysiology,)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 167 - 173 , 2017 , 1521-6616 ,

    초록

    Abstract Persistent stimulation with antigens derived from viruses that establish chronic infections or tumour antigens results in the exhaustion of T cells. Coinhibitory receptors like PD-1 and CTLA-4 function as immune checkpoints on exhausted T cells. Blocking these molecules with antibodies improve immunity to cancer cells. Immune checkpoint inhibitors targeting other coinhibitory receptors might have a similar role in improving T cell function and thus also utility in cancer therapy. Using HIV-specific T cells as a model for exhaustion we have evaluated the capacity of antibodies targeting TIM-3, BTLA, CD160, LAG-3 and CTLA-4 alone or in combination with a PD-1 antibody to enhance proliferation and cytokine production in response to Gag and Nef peptides. Antibodies targeting BTLA and TIM-3 enhanced CD8 T cell proliferation. Moreover, our results indicate that blocking BTLA and TIM-3 in combination with PD-1 might be especially effective in enhancing responses of exhausted human T cells. Highlights PD-1 blockade has a unique potency to enhance T cell response to HIV-1 antigens. BTLA and TIM-3 blockade can augment the PD-1 effect. Combination of immune checkpoint inhibitors could enhance their therapeutic potential. Graphical abstract [DISPLAY OMISSION]

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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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  4. [해외논문]   Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues   SCI SCIE SCOPUS

    Zhou, Zejun (Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29425, USA ) , Zhang, Lumin (Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA ) , Ding, Miao (Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29425, USA ) , Luo, Zhenwu (Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29425, USA ) , Yuan, Shao (The Biorepository & Tissue Analysis Shared Resource, Hollings Cancer Center, Medical University of South Carolina, SC 29425, USA ) , Bansal, Meena B. (Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA ) , Gilkeson, Gary (Division of Rheumatology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA ) , Lang, Ren (Department of Hepatobiliary Surgery, Beijing Chaoyang Hospital, Capital Medical University, Chaoyang Qu, Beijing 10020, China ) , Jiang, Wei (Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29425, USA)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 174 - 180 , 2017 , 1521-6616 ,

    초록

    Abstract Females have a higher prevalence of most autoimmune diseases; however, the mechanism is unknown. In this study, we examined the expression of tight junction protein zonula occludens 1 (ZO-1) and estrogen receptor (ER)-α/β in human primary gut tissues by immunohistochemistry, immunofluorescence and qPCR. The expression of ZO-1 and ER-β but not ER-α was present in both male and female gut tissues. There was no sex difference in ER-β expression, but ZO-1 expression was decreased in females compared to males. In vitro , estrogen treatment decreased ZO-1 mRNA and protein expression, ZO-1 promoter activity, IL-6 production, and NF-κB activation in human primary gut tissues or the Caco-2 cells, but increased the ER-β expression in Caco-2 cells. Consistently, plasma IL-6 levels in females were reduced relative to males in vivo . Our finding indicates that estrogen may play a role in gut tight junction expression and permeability.

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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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  5. [해외논문]   Hematologic neoplasms: Dendritic cells vaccines in motion   SCI SCIE SCOPUS

    Galati, Domenico (Corresponding author.) , Zanotta, Serena
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 181 - 190 , 2017 , 1521-6616 ,

    초록

    Abstract Dendritic cells (DCs) are bone-marrow-derived immune cells accounted for a key role in cancer vaccination as potent antigen-presenting cells within the immune system. Cancer microenvironment can modulate DCs maturation resulting in their accumulation into functional states associated with a reduced antitumor immune response. In this regard, a successful cancer vaccine needs to mount a potent antitumor immune response able to overcome the immunosuppressive tumor milieu. As a consequence, DCs-based approaches are a safe and promising strategy for improving the therapeutic efficacy in hematological malignancies, particularly in combinations with additional treatments. This review summarizes the most significant evidence about the immunotherapeutic strategies performed to target hematologic neoplasms including the tumoral associated antigens (TAA) pulsed on DCs, whole tumor cell vaccines or leukemia-derived DCs.

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  6. [해외논문]   HLA class Ia and Ib molecules and FOXP3+ TILs in relation to the prognosis of malignant melanoma patients   SCI SCIE SCOPUS

    Melsted, Wenna Nascimento (Centre for Immune Regulation and Reproductive Immunology (CIRRI), Department of Clinical Biochemistry, Zealand University Hospital, DK-4000 Roskilde, Denmark ) , Johansen, Lasse Lindholm (Centre for Immune Regulation and Reproductive Immunology (CIRRI), Department of Clinical Biochemistry, Zealand University Hospital, DK-4000 Roskilde, Denmark ) , Lock-Andersen, Jørgen (Department of Plastic Surgery, Zealand University Hospital, Roskilde, Denmark ) , Behrendt, Nille (Department of Pathology, Zealand University Hospital, Denmark ) , Eriksen, Jens Ole (Department of Pathology, Zealand University Hospital, Denmark ) , Bzorek, Michael (Department of Pathology, Zealand University Hospital, Denmark ) , Scheike, Thomas (Department of Biostatistics, University of Copenhagen, Denmark ) , Hviid, Thomas Vauvert F. (Centre for Immune Regulation and Reproductive Immunology (CIRRI), Department of Clinical Biochemistry, Zealand University Hospital, DK-4000 Roskilde, Denmark)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 191 - 197 , 2017 , 1521-6616 ,

    초록

    Abstract HLA class Ia (HLA-ABC) and HLA class Ib (HLA-E, -F and -G) molecules and FOXP3+ tumor-infiltrating lymphocytes (TILs) are often reported as relevant factors of tumor immune regulation. We investigated their expression as prognostic factors in 200 patients with primary cutaneous melanoma (PCM). In our cohort, patients with tumors showing upregulation of HLA-ABC molecules had significantly thicker tumors (32% vs 7%, P P = 0.007) and frequent nodular melanomas (20% vs 4%, P = 0.001). Additionally, high expression of HLA-G in the tumor was a sign of bad prognosis for the patients, being associated with thick tumors (30% vs 12%, P = 0.017), ulceration (24% vs 5%, P P = 0.015). HLA-E, HLA-F and FOXP3+ TILs were not indicative of the prognosis in PCM. High HLA-ABC and HLA-G were associated with tumor aggressiveness and could be relevant predictive markers for effective immunotherapy of melanoma tumors. Highlights Melanoma tumors are more aggressive when expressing high levels of HLA-ABC and HLA-G. HLA-G expression is correlated with a high number of FOXP3+ lymphocytes in the tumor. High HLA-ABC expression is associated with bad prognostic factors.

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

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  7. [해외논문]   A novel mutation in the JH4 domain of JAK3 causing severe combined immunodeficiency complicated by vertebral osteomyelitis   SCI SCIE SCOPUS

    Qamar, Farah (Department of Pediatric and Child Health, Aga Khan University Hospital, Pakistan ) , Junejo, Samina (Department of Pediatric and Child Health, Aga Khan University Hospital, Pakistan ) , Qureshi, Sonia (Department of Pediatric and Child Health, Aga Khan University Hospital, Pakistan ) , Seleman, Michael (Department of Allergy and immunology, Boston Children's Hospital, United States ) , Bainter, Wayne (Department of Allergy and immunology, Boston Children's Hospital, United States ) , Massaad, Michel (Department of Allergy and immunology, Boston Children's Hospital, United States ) , Chou, Janet (Department of Allergy and immunology, Boston Children's Hospital, United States ) , Geha, Raif S. (Department of Allergy and immunology, Boston Children's Hospital, United States)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 198 - 200 , 2017 , 1521-6616 ,

    초록

    Abstract JAK3 is a tyrosine kinase essential for signaling downstream of the common gamma chain subunit shared by multiple cytokine receptors. JAK3 deficiency results in T − B + NK − severe combined immune deficiency (SCID). We report a patient with SCID due to a novel mutation in the JAK3 JH4 domain. The function of the JH4 domain remains unknown. This is the first report of a missense mutation in the JAK3 JH4 domain, thereby demonstrating the importance of the JH4 domain of JAK3 in host immunity. Highlights We report the first missense mutation in the JAK3 JH4 domain in a patient with SCID. An intact JH4 domain of JAK3 is essential for adaptive immunity.

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  8. [해외논문]   Cernunnos deficiency associated with BCG adenitis and autoimmunity: First case from the national Iranian registry and review of the literature   SCI SCIE SCOPUS

    Yazdani, Reza (Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran ) , Abolhassani, Hassan (Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Science, Tehran, Iran ) , Tafaroji, Javad (Department of Pediatrics, Qom University of Medical Sciences, Qom, Iran ) , Azizi, Gholamreza (Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran ) , Hamidieh, Amir Ali (Hematology, Oncology and Stem Cell Transplantation Research Centre, Tehran University of Medical Sciences, Tehran, Iran ) , Chou, Janet (Division of Immunology Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, USA ) , Geha, Raif S. (Division of Immunology Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, USA ) , Aghamohammadi, Asghar (Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Science, Tehran, Iran)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 201 - 206 , 2017 , 1521-6616 ,

    초록

    Abstract Non-homologous end-joining (NHEJ) is a pathway that repairs double-strand breaks (DSB) in DNA and plays a vital role in V(D)J recombination of immunoglobulin genes. Cernunnos is a DNA repair factor that is involved in nonhomologous end-joining (NHEJ) process. Impairment in Cernunnos leads to a genetic disease characterized by neural disorders, immunodeficiency and increased radiosensitivity. We herein describe a severe combined immunodeficiency (SCID) patient with T- B+ phenotype who had a mutation in Cernunnos gene and manifested recurrent infections, microcephaly and growth retardation with hypogammaglobulinemia. Furthermore, our patient was associated with BCG adenitis and autoimmunity that less is observed in patients with Cernunnos deficiency. In contrast to previous reported Cernunnos-deficient patients, our patient had normal B-cell number along with normal IgA and IgM, suggesting a leaky form of the Cernunnos deficiency due to residual count of B cells in our patient. Cernunnos deficiency should be considered in children with recurrent bacterial infections, microcephaly and growth retardation, in spite of having normal B-cell as well as normal IgM and IgA level. Highlights A severe combined immunodeficiency (SCID) patient with T- B+ phenotype who had a mutation in Cernunnos gene The patient was associated with BCG adenitis and autoimmunity that less is observed in patients with Cernunnos deficiency Our patient had BCG adenitis and autoimmunity Normal B-cell, IgA and IgM suggesting a leaky form of the Cernunnos deficiency

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

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  9. [해외논문]   IL-17 and IFN-γ producing NK and γδ-T cells are preferentially expanded in synovial fluid of patients with reactive arthritis and undifferentiated spondyloarthritis   SCI SCIE SCOPUS

    Chowdhury, Abhra Chandra (Corresponding author.) , Chaurasia, Smriti , Mishra, Shravan Kumar , Aggarwal, Amita , Misra, Ramnath
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 207 - 212 , 2017 , 1521-6616 ,

    초록

    Abstract The IL-17/1L-23 axis is important in the pathogenesis of spondyloarthropathy. Innate cells produce IL-17 in addition to Th17 cells. We studied the frequencies of natural killer (NK) (total, CD56 bright , CD56 dim , perforin+ and granzyme+), NK-T, γδ-T, and IFN-γ+, IL-17+ NK and γδ-T cells in peripheral blood (PB) and synovial fluid (SF) of ReA/uSpA patients. PB from 45 patients and paired SF from 39 patients were studied, together with PB from 18 healthy controls (HC). The frequency of γδ-T cells was decreased (p bright NK cells were increased (p

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  10. [해외논문]   The gut microbiome and microbial translocation in multiple sclerosis   SCI SCIE SCOPUS

    Mirza, Ali (Department of Microbiology and Immunology, University of Michigan School of Medicine, 4258 Alfred Taubman Biomedical Sciences Research Bldg. 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, United States ) , Mao-Draayer, Yang (Department of Neurology, University of Michigan School of Medicine, 4015 Alfred Taubman Biomedical Sciences Research Bldg. 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, United States)
    Clinical immunology : the official journal of the Clinical Immunology Society v.183 ,pp. 213 - 224 , 2017 , 1521-6616 ,

    초록

    Abstract Individuals with multiple sclerosis (MS) have a distinct intestinal microbial community (microbiota) and increased low-grade translocation of bacteria from the intestines into the circulation. The observed change of intestinal bacteria in MS patients regulate immune functions involved in MS pathogenesis. These functions include: systemic and central nervous system (CNS) immunity (including peripheral regulatory T cell function), the blood-brain barrier (BBB) permeability and CNS-resident cell activity. This review discusses the MS intestinal microbiota implication on MS systemic- and CNS-immunopathology. We introduce the possible contributions of MS low-grade microbial translocation (LG-MT) to the development of MS, and end on a discussion on microbiota therapies for MS patients.

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