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Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica

Neuromyelitis optica (NMO) is an inflammatory disease affecting the optic nerve and spinal cord, in which autoantibodies against aquaporin 4 (AQP4) water channel protein probably play a pathogenic role. Here we show that a B-cell subpopulation, exhibiting the CD19(int)CD27(high)CD38(high)CD180(-) ph... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America 01 March 2011, Vol.108(9), pp.3701-6
Main Author: Chihara, Norio
Other Authors: Aranami, Toshimasa , Sato, Wakiro , Miyazaki, Yusei , Miyake, Sachiko , Okamoto, Tomoko , Ogawa, Masafumi , Toda, Tatsushi , Yamamura, Takashi
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; PMID: 21321193 Version:1 ; DOI: 10.1073/pnas.1017385108
Link: http://pubmed.gov/21321193
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recordid: medline21321193
title: Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica
format: Article
creator:
  • Chihara, Norio
  • Aranami, Toshimasa
  • Sato, Wakiro
  • Miyazaki, Yusei
  • Miyake, Sachiko
  • Okamoto, Tomoko
  • Ogawa, Masafumi
  • Toda, Tatsushi
  • Yamamura, Takashi
subjects:
  • Signal Transduction
  • Aquaporin 4 -- Immunology
  • Autoantibodies -- Biosynthesis
  • Interleukin-6 -- Metabolism
  • Neuromyelitis Optica -- Immunology
  • Plasma Cells -- Immunology
ispartof: Proceedings of the National Academy of Sciences of the United States of America, 01 March 2011, Vol.108(9), pp.3701-6
description: Neuromyelitis optica (NMO) is an inflammatory disease affecting the optic nerve and spinal cord, in which autoantibodies against aquaporin 4 (AQP4) water channel protein probably play a pathogenic role. Here we show that a B-cell subpopulation, exhibiting the CD19(int)CD27(high)CD38(high)CD180(-) phenotype, is selectively increased in the peripheral blood of NMO patients and that anti-AQP4 antibodies (AQP4-Abs) are mainly produced by these cells in the blood of these patients. These B cells showed the morphological as well as the phenotypical characteristics of plasmablasts (PB) and were further expanded during NMO relapse. We also demonstrate that interleukin 6 (IL-6), shown to be increased in NMO, enhanced the survival of PB as well as their AQP4-Ab secretion, whereas the blockade of IL-6 receptor (IL-6R) signaling by anti-IL-6R antibody reduced the survival of PB in vitro. These results indicate that the IL-6-dependent B-cell subpopulation is involved in the pathogenesis of NMO, thereby...
language: eng
source:
identifier: E-ISSN: 1091-6490 ; PMID: 21321193 Version:1 ; DOI: 10.1073/pnas.1017385108
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleInterleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica
creatorChihara, Norio ; Aranami, Toshimasa ; Sato, Wakiro ; Miyazaki, Yusei ; Miyake, Sachiko ; Okamoto, Tomoko ; Ogawa, Masafumi ; Toda, Tatsushi ; Yamamura, Takashi
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subjectSignal Transduction ; Aquaporin 4 -- Immunology ; Autoantibodies -- Biosynthesis ; Interleukin-6 -- Metabolism ; Neuromyelitis Optica -- Immunology ; Plasma Cells -- Immunology
descriptionNeuromyelitis optica (NMO) is an inflammatory disease affecting the optic nerve and spinal cord, in which autoantibodies against aquaporin 4 (AQP4) water channel protein probably play a pathogenic role. Here we show that a B-cell subpopulation, exhibiting the CD19(int)CD27(high)CD38(high)CD180(-) phenotype, is selectively increased in the peripheral blood of NMO patients and that anti-AQP4 antibodies (AQP4-Abs) are mainly produced by these cells in the blood of these patients. These B cells showed the morphological as well as the phenotypical characteristics of plasmablasts (PB) and were further expanded during NMO relapse. We also demonstrate that interleukin 6 (IL-6), shown to be increased in NMO, enhanced the survival of PB as well as their AQP4-Ab secretion, whereas the blockade of IL-6 receptor (IL-6R) signaling by anti-IL-6R antibody reduced the survival of PB in vitro. These results indicate that the IL-6-dependent B-cell subpopulation is involved in the pathogenesis of NMO, thereby...
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titleInterleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica
descriptionNeuromyelitis optica (NMO) is an inflammatory disease affecting the optic nerve and spinal cord, in which autoantibodies against aquaporin 4 (AQP4) water channel protein probably play a pathogenic role. Here we show that a B-cell subpopulation, exhibiting the CD19(int)CD27(high)CD38(high)CD180(-) phenotype, is selectively increased in the peripheral blood of NMO patients and that anti-AQP4 antibodies (AQP4-Abs) are mainly produced by these cells in the blood of these patients. These B cells showed the morphological as well as the phenotypical characteristics of plasmablasts (PB) and were further expanded during NMO relapse. We also demonstrate that interleukin 6 (IL-6), shown to be increased in NMO, enhanced the survival of PB as well as their AQP4-Ab secretion, whereas the blockade of IL-6 receptor (IL-6R) signaling by anti-IL-6R antibody reduced the survival of PB in vitro. These results indicate that the IL-6-dependent B-cell subpopulation is involved in the pathogenesis of NMO, thereby...
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abstractNeuromyelitis optica (NMO) is an inflammatory disease affecting the optic nerve and spinal cord, in which autoantibodies against aquaporin 4 (AQP4) water channel protein probably play a pathogenic role. Here we show that a B-cell subpopulation, exhibiting the CD19(int)CD27(high)CD38(high)CD180(-) phenotype, is selectively increased in the peripheral blood of NMO patients and that anti-AQP4 antibodies (AQP4-Abs) are mainly produced by these cells in the blood of these patients. These B cells showed the morphological as well as the phenotypical characteristics of plasmablasts (PB) and were further expanded during NMO relapse. We also demonstrate that interleukin 6 (IL-6), shown to be increased in NMO, enhanced the survival of PB as well as their AQP4-Ab secretion, whereas the blockade of IL-6 receptor (IL-6R) signaling by anti-IL-6R antibody reduced the survival of PB in vitro. These results indicate that the IL-6-dependent B-cell subpopulation is involved in the pathogenesis of NMO, thereby...
doi10.1073/pnas.1017385108
pmid21321193
date2011-03-01