KMID : 0923620190190040027
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Immune Network 2019 Volume.19 No. 4 p.27 ~ p.27
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Intravenous Immunoglobulin Controls Th17 Cell-Mediated Osteoclastogenesis
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Kim Kyoung-Woon
Kim Hae-Rim Kim Bo-Mi Won Ji-Yeon Lee Kyung-Ann Lee Sang-Heon
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Abstract
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The purpose of this study was to determine the regulatory role of intravenous Ig (IVIg) in Th17 cytokine?induced RANK ligand (RANKL) expression and osteoclast (OC) differentiation from OC precursors (pre-OC). Human CD14+ monocytes were isolated and stimulated by Th17 cytokines (IL-17, IL-21, and IL-22) and RANKL expression was investigated using a real-time PCR. CD14+ monocytes were incubated with RANKL, Th17 cytokines, and M-CSF, with/without IVIg, and OC differentiation was determined by counting tartrate-resistant acid phosphatase-positive multinucleated cells. OC differentiation was investigated after monocytes were cocultured with Th17 cells in the presence of IVIg. Th17 cell differentiation was determined using enzyme-linked immunosorbent assay and flow cytometry after CD4+ T cells were cultured with IVIg under Th17 condition. Th17 cytokines stimulated monocytes to express RANKL and IVIg suppressed the Th17 cytokine-induced RANKL expression. OCs were differentiated when pre-OC were cocultured with RANKL or Th17 cytokines and IVIg reduced the osteoclastogenesis. IVIg also decreased osteoclastogenesis when pre-OC were cocultured with Th17 cells. IVIg decreased both Th17 and Th1 cell differentiation while it did not affect Treg cell differentiation. In summary, IVIg inhibited Th17 cytokine-induced RANKL expression and OC differentiation. IVIg reduced osteoclastogenesis when monocytes were cocultured with Th17 cells. IVIg also reduced Th17 polarization. IVIg could be a new therapeutic option for Th17 cell?mediated osteoclastogenesis.
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KEYWORD
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IVIg, Osteoclastogenesis, RANK ligand, IL-17, Th17 cells
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