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Article: Natural killer cell degeneration exacerbates experimental arthritis in mice via enhanced interleukin-17 production

TitleNatural killer cell degeneration exacerbates experimental arthritis in mice via enhanced interleukin-17 production
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
Citation
Arthritis And Rheumatism, 2008, v. 58 n. 9, p. 2700-2711 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/129527
ISSN
2014 Impact Factor: 7.764
2014 SCImago Journal Rankings: 2.103
ISI Accession Number ID
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.

References

 

DC FieldValueLanguage
dc.contributor.authorLo, CKCen_HK
dc.contributor.authorLam, QLKen_HK
dc.contributor.authorSun, Len_HK
dc.contributor.authorWang, Sen_HK
dc.contributor.authorKo, KHen_HK
dc.contributor.authorXu, Hen_HK
dc.contributor.authorWu, CYen_HK
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorLu, Len_HK
dc.date.accessioned2010-12-23T08:38:27Z-
dc.date.available2010-12-23T08:38:27Z-
dc.date.issued2008en_HK
dc.identifier.citationArthritis And Rheumatism, 2008, v. 58 n. 9, p. 2700-2711en_HK
dc.identifier.issn0004-3591en_HK
dc.identifier.urihttp://hdl.handle.net/10722/129527-
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.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/en_HK
dc.relation.ispartofArthritis and Rheumatismen_HK
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 productionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0004-3591&volume=58&issue=9&spage=2700&epage=2711&date=2008&atitle=Natural+killer+cell+degeneration+exacerbates+experimental+arthritis+in+mice+via+enhanced+interleukin-17+production-
dc.identifier.emailLam, QLK: qlam@pathology.hku.hken_HK
dc.identifier.emailZheng, BJ: bzheng@hkucc.hku.hken_HK
dc.identifier.emailLu, L: liweilu@hkucc.hku.hken_HK
dc.identifier.authorityLam, QLK=rp00312en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1002/art.23760en_HK
dc.identifier.pmid18759269en_HK
dc.identifier.scopuseid_2-s2.0-51849147995en_HK
dc.identifier.hkuros176937en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51849147995&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume58en_HK
dc.identifier.issue9en_HK
dc.identifier.spage2700en_HK
dc.identifier.epage2711en_HK
dc.identifier.eissn1529-0131-
dc.identifier.isiWOS:000259244000015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLo, CKC=24825171000en_HK
dc.identifier.scopusauthoridLam, QLK=8722491000en_HK
dc.identifier.scopusauthoridSun, L=35265069800en_HK
dc.identifier.scopusauthoridWang, S=23500575700en_HK
dc.identifier.scopusauthoridKo, KH=7202688627en_HK
dc.identifier.scopusauthoridXu, H=7407449104en_HK
dc.identifier.scopusauthoridWu, CY=7501660961en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridLu, L=7403963552en_HK

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