About: Collagen-induced arthritis: severity and immune response attenuation using multivalent N-acetyl glucosamine     Goto   Sponge   NotDistinct   Permalink

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  • Rheumatoid arthritis is an autoimmunity leading to considerable impairment of quality of life. N-acetyl glucosamine (GlcNAc) has been described previously as a potent modulator of experimental arthritis in animal models and is used for osteoarthritis treatment in humans, praised for its lack of adverse effects. In this study we present a comprehensive immunological analysis of multivalent GlcNAc-terminated glycoconjugate (GC) application in the treatment of collagen-induced arthritis (CIA) and its clinical outcome. We used immunohistochemistry and FACS to describe conditions on the inflammation site. Systemic and clinical effects were evaluated by FACS, cytotoxicity assay, ELISA, cytometric bead array (CBA), RT-PCR and clinical scoring. We found reduced inflammatory infiltration, NKG2D expression on NK and suppression of T, B and antigen-presenting cells (APC) in the synovia. On the systemic level, GCs prevented the activation of monocyte- and B cell-derived APCs, the rise of TNF- and IFN- levels, and subsequent type II collagen (CII)-specific IgG2a formation. Moreover, we detected an increase of anti-inflammatory IL-4 mRNA in the spleen. Similar to the synovia, the GCs caused a significant reduction of NKG2D-expressing NK cells in the spleen without influencing their lytic function.
  • Rheumatoid arthritis is an autoimmunity leading to considerable impairment of quality of life. N-acetyl glucosamine (GlcNAc) has been described previously as a potent modulator of experimental arthritis in animal models and is used for osteoarthritis treatment in humans, praised for its lack of adverse effects. In this study we present a comprehensive immunological analysis of multivalent GlcNAc-terminated glycoconjugate (GC) application in the treatment of collagen-induced arthritis (CIA) and its clinical outcome. We used immunohistochemistry and FACS to describe conditions on the inflammation site. Systemic and clinical effects were evaluated by FACS, cytotoxicity assay, ELISA, cytometric bead array (CBA), RT-PCR and clinical scoring. We found reduced inflammatory infiltration, NKG2D expression on NK and suppression of T, B and antigen-presenting cells (APC) in the synovia. On the systemic level, GCs prevented the activation of monocyte- and B cell-derived APCs, the rise of TNF- and IFN- levels, and subsequent type II collagen (CII)-specific IgG2a formation. Moreover, we detected an increase of anti-inflammatory IL-4 mRNA in the spleen. Similar to the synovia, the GCs caused a significant reduction of NKG2D-expressing NK cells in the spleen without influencing their lytic function. (en)
Title
  • Collagen-induced arthritis: severity and immune response attenuation using multivalent N-acetyl glucosamine
  • Collagen-induced arthritis: severity and immune response attenuation using multivalent N-acetyl glucosamine (en)
skos:prefLabel
  • Collagen-induced arthritis: severity and immune response attenuation using multivalent N-acetyl glucosamine
  • Collagen-induced arthritis: severity and immune response attenuation using multivalent N-acetyl glucosamine (en)
skos:notation
  • RIV/61388971:_____/14:00435665!RIV15-GA0-61388971
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • I, P(GA310/06/0477), P(GD310/08/H077)
http://linked.open...iv/cisloPeriodika
  • 1
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  • 7724
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  • RIV/61388971:_____/14:00435665
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  • CIA; clinical scoring; cytokines (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • GB - Spojené království Velké Británie a Severního Irska
http://linked.open...ontrolniKodProRIV
  • [6845BD824E56]
http://linked.open...i/riv/nazevZdroje
  • Clinical and Experimental Immunology
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http://linked.open...ichTvurcuVysledku
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  • 177
http://linked.open...iv/tvurceVysledku
  • Vannucci, Luca
  • Fišerová, Anna
  • Richter, Jan
  • Malý, M.
  • Dányi, István
  • Hříbalová, Věra
  • Čapková, Katarína
http://linked.open...ain/vavai/riv/wos
  • 000337588700013
issn
  • 0009-9104
number of pages
http://bibframe.org/vocab/doi
  • 10.1111/cei.12313
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