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We are analyzing https://link.springer.com/article/10.1007/s10157-010-0309-9.

Title:
Involvement of CD11b+ GR-1low cells in autoimmune disorder in MRL-Fas lpr mouse | Clinical and Experimental Nephrology
Description:
Objective Myeloid-derived suppressor cells (MDSCs) have been identified as immunosuppressive cells in tumor-related inflammation. However, the pathogenesis of MDSCs for autoimmune disease has not been investigated as yet. The aim of this study was to address whether MDSCs contribute to autoimmune organ injury in lupus-prone mice. Methods MDSCs were analyzed by flow cytometric staining of CD11b+ GR-1+ in MRL-Fas lpr mice. CD4+ T-cell proliferation assay was performed by coculture with CD11b+ GR-1+ splenocytes. The percentage of immunosuppressive cells was examined during disease progression. Expression of chemokine receptor on immunosuppressive cells was analyzed, and chemotaxis assay was performed. Results CD11b+ GR-1low cells had a suppressive effect on CD4+ T-cell proliferation, which was restored by an arginase-1 inhibitor. CD11b+ GR-1low cells increased in percentage during disease progression in kidney and blood. The number of migrated CD11b+ GR-1low cells increased in the presence of monocyte chemoattractant protein-1/CCL2. Conclusion We assessed the involvement of CD11b+ GR-1low cells in autoimmune disorder in MRL-Fas lpr mice. These cells regulate immunological responses via CCL2/CCR2 signaling. The regulation of immunosuppressive monocytes may provide novel therapeutic strategy for organ damage in autoimmune diseases.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Health & Fitness
  • Education

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {πŸ“ˆ}

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We don't see any clear sign of profit-making.

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Keywords {πŸ”}

cells, article, scholar, google, pubmed, cas, suppressor, autoimmune, cdb, mice, access, grlow, myeloidderived, disease, myeloid, immunol, privacy, cookies, content, mrlfas, lpr, wada, mdscs, immunosuppressive, cancer, japan, publish, search, iwata, furuichi, satoshi, sakai, ueha, matsushima, regulation, open, stem, rev, clin, nephrol, medicine, kanazawa, data, information, log, journal, research, experimental, involvement, disorder,

Topics {βœ’οΈ}

mrl/lpr lupus-prone mice month download article/chapter mrl-fas lpr mouse myeloid-derived suppressor cells cd11b+ gr-1low cells mrl-fas lpr mice monocyte chemoattractant protein-1/ccl2 cd4+ t-cell proliferation chemokine-mediated rapid turnover ccl2/ccr2 signaling establish long-lasting contact lung immune cells lupus-prone mice pleiotropic-inflamed monocytes/macrophages myeloid suppressor cells autoimmune renal injury tumor-induced tolerance systemic lupus erythematosus related subjects tumor-related inflammation full article pdf autoimmune organ injury autoimmune effector cells cd11b+ gr-1+ splenocytes privacy choices/manage cookies tumor-bearing mice check access instant access autoimmune diseases cd11b+ly-6c article iwata experimental nephrology aims m2 macrophage programming experimental autoimmune encephalomyelitis chronic contact eczema article clinical inflammatory cell infiltration european economic area flow cytometric staining m2-type characteristics talmadge je chemokine receptor conditions privacy policy inflammatory bowel disease cd11b+ gr-1+ article log accepting optional cookies molecular preventive medicine takeda science foundation cancer metastasis rev

Schema {πŸ—ΊοΈ}

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         headline:Involvement of CD11b+ GR-1low cells in autoimmune disorder in MRL-Fas lpr mouse
         description:Myeloid-derived suppressor cells (MDSCs) have been identified as immunosuppressive cells in tumor-related inflammation. However, the pathogenesis of MDSCs for autoimmune disease has not been investigated as yet. The aim of this study was to address whether MDSCs contribute to autoimmune organ injury in lupus-prone mice. MDSCs were analyzed by flow cytometric staining of CD11b+ GR-1+ in MRL-Fas lpr mice. CD4+ T-cell proliferation assay was performed by coculture with CD11b+ GR-1+ splenocytes. The percentage of immunosuppressive cells was examined during disease progression. Expression of chemokine receptor on immunosuppressive cells was analyzed, and chemotaxis assay was performed. CD11b+ GR-1low cells had a suppressive effect on CD4+ T-cell proliferation, which was restored by an arginase-1 inhibitor. CD11b+ GR-1low cells increased in percentage during disease progression in kidney and blood. The number of migrated CD11b+ GR-1low cells increased in the presence of monocyte chemoattractant protein-1/CCL2. We assessed the involvement of CD11b+ GR-1low cells in autoimmune disorder in MRL-Fas lpr mice. These cells regulate immunological responses via CCL2/CCR2 signaling. The regulation of immunosuppressive monocytes may provide novel therapeutic strategy for organ damage in autoimmune diseases.
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      headline:Involvement of CD11b+ GR-1low cells in autoimmune disorder in MRL-Fas lpr mouse
      description:Myeloid-derived suppressor cells (MDSCs) have been identified as immunosuppressive cells in tumor-related inflammation. However, the pathogenesis of MDSCs for autoimmune disease has not been investigated as yet. The aim of this study was to address whether MDSCs contribute to autoimmune organ injury in lupus-prone mice. MDSCs were analyzed by flow cytometric staining of CD11b+ GR-1+ in MRL-Fas lpr mice. CD4+ T-cell proliferation assay was performed by coculture with CD11b+ GR-1+ splenocytes. The percentage of immunosuppressive cells was examined during disease progression. Expression of chemokine receptor on immunosuppressive cells was analyzed, and chemotaxis assay was performed. CD11b+ GR-1low cells had a suppressive effect on CD4+ T-cell proliferation, which was restored by an arginase-1 inhibitor. CD11b+ GR-1low cells increased in percentage during disease progression in kidney and blood. The number of migrated CD11b+ GR-1low cells increased in the presence of monocyte chemoattractant protein-1/CCL2. We assessed the involvement of CD11b+ GR-1low cells in autoimmune disorder in MRL-Fas lpr mice. These cells regulate immunological responses via CCL2/CCR2 signaling. The regulation of immunosuppressive monocytes may provide novel therapeutic strategy for organ damage in autoimmune diseases.
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            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Satoshi Kokubo
      affiliation:
            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Kazuaki Shimizu
      affiliation:
            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Norihiko Sakai
      affiliation:
            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Akihiro Sagara
      affiliation:
            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Yukie Kurokawa
      affiliation:
            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Satoshi Ueha
      affiliation:
            name:University of Tokyo
            address:
               name:Department of Molecular Preventive Medicine, University of Tokyo, Tokyo, Japan
               type:PostalAddress
            type:Organization
      name:Kouji Matsushima
      affiliation:
            name:University of Tokyo
            address:
               name:Department of Molecular Preventive Medicine, University of Tokyo, Tokyo, Japan
               type:PostalAddress
            type:Organization
      name:Shuichi Kaneko
      affiliation:
            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Takashi Wada
      affiliation:
            name:Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University
            address:
               name:Department of Laboratory Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Molecular Preventive Medicine, University of Tokyo, Tokyo, Japan
      name:Department of Molecular Preventive Medicine, University of Tokyo, Tokyo, Japan
      name:Department of Disease Control and Homeostasis, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
      name:Department of Laboratory Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Faculty of Medicine, Kanazawa University, Kanazawa, Japan
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