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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Impaired inhibitory Fcγ receptor IIB expression on B cells in chronic inflammatory demyelinating polyneuropathy
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Impaired inhibitory Fcγ receptor IIB expression on B cells in chronic inflammatory demyelinating polyneuropathy

机译：慢性炎症性脱髓鞘性多发性神经病B细胞抑制性Fcγ受体IIB表达受损

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摘要

The inhibitory Fc-y receptor FcyRIIB, expressed on myeloid and B cells, has a critical role in the balance of tolerance and autoimmu-nity, and is required for the antiinflammatory activity of intravenous lg (IVIG) in various murine disease models. However, the function of FcγRIIB and its regulation by IVIG in human autoimmune diseases are less well understood. Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common treatable acquired chronic polyneuropathy, and IVIG is widely used as a first-line initial and maintenance treatment. We found that untreated patients with CIDP, compared with demographically matched healthy controls, showed consistently lower FcγRIIB expression levels on naive B cells, and failed to up-regulate or to maintain up-regulation of FcγRIIB as B cells progressed from the naive to the memory compartment. Concomitantly, the rare -386C/-120A FcγRIIB promoter polymorphism resulting in reduced promoter activity previously associated with autoimmune phenotypes was overrepresented in CIDP. Also, FcyRIIB protein expression was up-regulated on monocytes and B cells after clinically effective IVIG therapy. Thus, our results suggest that the inhibitory FcγRIIB is impaired at a critical B cell differentiation checkpoint in CIDP, and that modulating FcγRIIB expression might be a promising approach to efficiently limit antibody-mediated immunopathology in CIDP.
机译：在髓样细胞和B细胞上表达的抑制性Fc-γ受体FcyRIIB在耐受性和自身免疫性的平衡中起关键作用，并且是各种鼠类疾病模型中静脉注射IgG（IVIG）的抗炎活性所必需的。然而，人们对FcγRIIB的功能及其在人自身免疫性疾病中受IVIG的调节的了解还很少。慢性炎性脱髓鞘性多发性神经病（CIDP）是最常见的可治疗性获得性慢性多发性神经病，IVIG被广泛用作一线初始和维持治疗。我们发现与人口统计学匹配的健康对照相比，未经治疗的CIDP患者在幼稚B细胞上显示出始终较低的FcγRIIB表达水平，并且随着B细胞从幼稚期发展到记忆，未能上调或维持FcγRIIB的上调隔间。同时，在CIDP中过分代表了罕见的-386C / -120AFcγRIIB启动子多态性，导致先前与自身免疫表型有关的启动子活性降低。此外，临床上有效的IVIG治疗后，单核细胞和B细胞上的FcyRIIB蛋白表达上调。因此，我们的结果表明抑制性FcγRIIB在CIDP的关键B细胞分化检查点受损，并且调节FcγRIIB的表达可能是有效限制CIDP中抗体介导的免疫病理学的一种有前途的方法。

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    Bjoern Tackenberg; Ilijas Jelcic; Anne Baerenwaldt; Wolfgang H. Oertel; Norbert Sommer; Falk Nimmerjahn; Jan D. Luenemann;

  • 作者单位

    Department of Neurology, Clinical Neuroimmunology Group, Philipps-University, 35039 Marburg, Germany;

    Institute for Neuroimmunology and Clinical Multiple Sclerosis Research Center for Molecular Neurobiology Hamburg, University Medical Center Eppendorf, 20251 Hamburg, Germany;

    Laboratory of Experimental Immunology and Immunotherapy, Nikolaus-Fiebiger-Center for Molecular Medicine, University of Erlangen-Nuremberg, 91054 Erlangen, Germany;

    Department of Neurology, Clinical Neuroimmunology Group, Philipps-University, 35039 Marburg, Germany;

    Department of Neurology, Clinical Neuroimmunology Group, Philipps-University, 35039 Marburg, Germany;

    Laboratory of Experimental Immunology and Immunotherapy, Nikolaus-Fiebiger-Center for Molecular Medicine, University of Erlangen-Nuremberg, 91054 Erlangen, Germany;

    Laboratory of Viral Immunobiology, Christopher H. Browne Center for Immunology and Immune Diseases, The Rockefeller University, New York, NY 10065 Institute of Experimental Immunology, Viral Immunobiology, University Hospital of Zuerich, Zuerich, Switzerland;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    autoimmunity; human; immunology; Fc receptor; CIDP;

    机译：自身免疫人免疫学Fc受体;国际开发计划署;

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