Publications
Detailed Information
Reciprocal cross-talk between RANKL and interferon-gamma-inducible protein 10 is responsible for bone-erosive experimental arthritis
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Seungbok | - |
dc.contributor.author | Kwak, Han Bok | - |
dc.contributor.author | Ha, Hyunil | - |
dc.contributor.author | Kim, Ha-Neui | - |
dc.contributor.author | Lee, Jong-Ho | - |
dc.contributor.author | Kim, Hun Soo | - |
dc.contributor.author | Kim, Hyun-Man | - |
dc.contributor.author | Kim, Jung Yeon | - |
dc.contributor.author | Kim, Hong-Hee | - |
dc.contributor.author | Song, Yeong Wook | - |
dc.contributor.author | Lee, Zang Hee | - |
dc.date.accessioned | 2010-09-05T22:59:58Z | - |
dc.date.available | 2010-09-05T22:59:58Z | - |
dc.date.issued | 2008-04 | - |
dc.identifier.citation | Arthritis & Rheumatism 2008;58:1332-1342 | en |
dc.identifier.issn | 0004-3591 | - |
dc.identifier.uri | https://hdl.handle.net/10371/69681 | - |
dc.description.abstract | Objective
Interferon--inducible protein 10 (IP-10; also called CXCL10), a chemokine important in the migration and proliferation of T cells, is induced in a wide variety of cell types. However, the role of IP-10 in rheumatoid arthritis (RA) remains largely unknown. The purpose of this study was to examine the potential role of IP-10 in bone resorption and RA through examination of a mouse model of collagen-induced arthritis (CIA). Methods The effects of IP-10 on mouse T cells during osteoclast differentiation were examined in migration assays. The bone-erosive activity of IP-10 was determined in vivo in a mouse model of CIA by histologic and immunostaining analyses. Cytokine levels in serum and culture medium were measured with sandwich enzyme-linked immunosorbent assays. Results Serum concentrations of IP-10 were significantly higher in mice with CIA than in control mice. RANKL greatly induced IP-10 expression in osteoclast precursors, but not in mature osteoclasts. IP-10 stimulated the expression of RANKL and tumor necrosis factor (TNF) in CD4+ T cells and induced osteoclastogenesis in cocultures of CD4+ T cells and osteoclast precursors. However, IP-10 did not induce RANKL or TNF in CD8+ T cells. Treatment with neutralizing antibody to IP-10 significantly inhibited the infiltration of CD4+ T cells and F4/80+ macrophages into the synovium and attenuated bone destruction in mice with CIA. Furthermore, levels of RANKL and TNF were inhibited by antibody to IP-10. Bone erosion was observed in mice infected with an IP-10 retrovirus. Conclusion Our findings suggest that IP-10 plays a critical role in the infiltration of CD4+ T cells and F4/80+ macrophages into inflamed joints and causes bone destruction. Our results provide the first evidence that IP-10 contributes to the recruitment of inflammatory cells and is involved in bone erosion in inflamed joints. | en |
dc.language.iso | en | en |
dc.publisher | Wiley-Blackwell | en |
dc.title | Reciprocal cross-talk between RANKL and interferon-gamma-inducible protein 10 is responsible for bone-erosive experimental arthritis | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 이승복 | - |
dc.contributor.AlternativeAuthor | 곽한복 | - |
dc.contributor.AlternativeAuthor | 하현일 | - |
dc.contributor.AlternativeAuthor | 김하늬 | - |
dc.contributor.AlternativeAuthor | 이종호 | - |
dc.contributor.AlternativeAuthor | 김현만 | - |
dc.contributor.AlternativeAuthor | 김정연 | - |
dc.contributor.AlternativeAuthor | 김홍희 | - |
dc.contributor.AlternativeAuthor | 송영욱 | - |
dc.contributor.AlternativeAuthor | 이장희 | - |
dc.identifier.doi | 10.1002/art.23372 | - |
- Appears in Collections:
- Files in This Item:
- There are no files associated with this item.
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.