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Article: Natural killer cell degeneration exacerbates experimental arthritis in mice via enhanced interleukin-17 production
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TitleNatural killer cell degeneration exacerbates experimental arthritis in mice via enhanced interleukin-17 production
 
AuthorsLo, CKC3
Lam, QLK3
Sun, L2
Wang, S1
Ko, KH3
Xu, H1
Wu, CY4
Zheng, BJ3
Lu, L3
 
Issue Date2008
 
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
 
CitationArthritis And Rheumatism, 2008, v. 58 n. 9, p. 2700-2711 [How to Cite?]
DOI: http://dx.doi.org/10.1002/art.23760
 
AbstractObjective. An altered phenotype and dysfunction of natural killer (NK) cells have been observed in patients with rheumatoid arthritis. The aim of this study was to determine whether dysregulated NK cells contribute to the pathogenesis of experimental arthritis. Methods. For initiation of collagen-induced arthritis (CIA), DBA/1J mice were immunized with type II collagen in Freund's adjuvant. Control mice were immunized with adjuvant alone. NK cells from the blood, spleens, and bone marrow of immunized mice were analyzed by flow cytometry. Levels of interleukin-17 (IL-17) secretion and autoantibody production were measured by enzyme-linked immunosorbent assays. Immunized mice in which NK cells were depleted by anti-asialo GM1 antibody treatment were assessed for the development of CIA. Moreover, sorting-purified NK cells from both mice with CIA and control mice were analyzed for cytokine gene expression. Results. We observed markedly reduced frequencies of NK cells in the blood and spleens of mice with CIA compared with the frequencies in adjuvant-treated control mice. Upon NK cell depletion, immunized mice displayed an early onset of arthritis with more severe clinical symptoms, which correlated with increased plasma cell generation and autoantibody production. Moreover, a substantially increased number of IL-17-secreting cells in synovial tissue and more pronounced joint damage were observed. Freshly isolated NK cells from mice with CIA showed markedly reduced expression of interferon-γ (IFNγ). Furthermore, coculture of normal NK cells and CD4+ T cells revealed that NK cells strongly suppressed production of Th17 cells via their IFNγ production. Conclusion. These results suggest that NK cells play a protective role in the development of experimental arthritis, an effect that is possibly mediated by suppressing Th17 cell generation via IFNγ production. © 2008, American College of Rheumatology.
 
ISSN0004-3591
2013 Impact Factor: 7.871
 
DOIhttp://dx.doi.org/10.1002/art.23760
 
ISI Accession Number IDWOS:000259244000015
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU7423/04M
Funding Information:

Dr. Lu'S work was supported by grant HKU7423/04M from the Research Grants Council of Hong Kong.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLo, CKC
 
dc.contributor.authorLam, QLK
 
dc.contributor.authorSun, L
 
dc.contributor.authorWang, S
 
dc.contributor.authorKo, KH
 
dc.contributor.authorXu, H
 
dc.contributor.authorWu, CY
 
dc.contributor.authorZheng, BJ
 
dc.contributor.authorLu, L
 
dc.date.accessioned2010-12-23T08:38:27Z
 
dc.date.available2010-12-23T08:38:27Z
 
dc.date.issued2008
 
dc.description.abstractObjective. An altered phenotype and dysfunction of natural killer (NK) cells have been observed in patients with rheumatoid arthritis. The aim of this study was to determine whether dysregulated NK cells contribute to the pathogenesis of experimental arthritis. Methods. For initiation of collagen-induced arthritis (CIA), DBA/1J mice were immunized with type II collagen in Freund's adjuvant. Control mice were immunized with adjuvant alone. NK cells from the blood, spleens, and bone marrow of immunized mice were analyzed by flow cytometry. Levels of interleukin-17 (IL-17) secretion and autoantibody production were measured by enzyme-linked immunosorbent assays. Immunized mice in which NK cells were depleted by anti-asialo GM1 antibody treatment were assessed for the development of CIA. Moreover, sorting-purified NK cells from both mice with CIA and control mice were analyzed for cytokine gene expression. Results. We observed markedly reduced frequencies of NK cells in the blood and spleens of mice with CIA compared with the frequencies in adjuvant-treated control mice. Upon NK cell depletion, immunized mice displayed an early onset of arthritis with more severe clinical symptoms, which correlated with increased plasma cell generation and autoantibody production. Moreover, a substantially increased number of IL-17-secreting cells in synovial tissue and more pronounced joint damage were observed. Freshly isolated NK cells from mice with CIA showed markedly reduced expression of interferon-γ (IFNγ). Furthermore, coculture of normal NK cells and CD4+ T cells revealed that NK cells strongly suppressed production of Th17 cells via their IFNγ production. Conclusion. These results suggest that NK cells play a protective role in the development of experimental arthritis, an effect that is possibly mediated by suppressing Th17 cell generation via IFNγ production. © 2008, American College of Rheumatology.
 
dc.description.naturepostprint
 
dc.identifier.citationArthritis And Rheumatism, 2008, v. 58 n. 9, p. 2700-2711 [How to Cite?]
DOI: http://dx.doi.org/10.1002/art.23760
 
dc.identifier.doihttp://dx.doi.org/10.1002/art.23760
 
dc.identifier.eissn1529-0131
 
dc.identifier.epage2711
 
dc.identifier.hkuros176937
 
dc.identifier.isiWOS:000259244000015
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU7423/04M
Funding Information:

Dr. Lu'S work was supported by grant HKU7423/04M from the Research Grants Council of Hong Kong.

 
dc.identifier.issn0004-3591
2013 Impact Factor: 7.871
 
dc.identifier.issue9
 
dc.identifier.openurl
 
dc.identifier.pmid18759269
 
dc.identifier.scopuseid_2-s2.0-51849147995
 
dc.identifier.spage2700
 
dc.identifier.urihttp://hdl.handle.net/10722/129527
 
dc.identifier.volume58
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofArthritis and Rheumatism
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.rightsArthritis & Rheumatism. Copyright © John Wiley & Sons, Inc.
 
dc.rightsThis is a preprint of an article published in Arthritis & Rheumatism, 2008, v. 58 n. 9, p. 2700-2711
 
dc.subject.meshAntibodies, Monoclonal - immunology
 
dc.subject.meshApoptosis - immunology
 
dc.subject.meshArthritis, Experimental - chemically induced - immunology - metabolism - pathology
 
dc.subject.meshInterleukin-17 - biosynthesis - immunology
 
dc.subject.meshKiller Cells, Natural - immunology - metabolism - pathology
 
dc.titleNatural killer cell degeneration exacerbates experimental arthritis in mice via enhanced interleukin-17 production
 
dc.typeArticle
 
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Author Affiliations
  1. Jiangsu University
  2. Nanjing University, School of Medicine
  3. The University of Hong Kong
  4. Sun Yat Sen University of Medical Sciences