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Mobilization of nat...
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Leavenworth, Jianmei W
(author)
Mobilization of natural killer cells inhibits development of collagen-induced arthritis.
- Article/chapterEnglish2011
Publisher, publication year, extent ...
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2011-08-22
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Proceedings of the National Academy of Sciences,2011
Numbers
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LIBRIS-ID:oai:gup.ub.gu.se/149527
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https://gup.ub.gu.se/publication/149527URI
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https://doi.org/10.1073/pnas.1112188108DOI
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Although natural killer (NK) cells have been implicated in regulating immune responses, their ability to modulate disease development in autoimmune arthritis has not been analyzed. Here we investigate the contribution of NK cells to regulating collagen-induced arthritis, a well-characterized preclinical model of human rheumatoid arthritis. We find that the disease is induced by the combined action of two CD4(+) T helper (T(H)) subsets: follicular T(H) cells and T(H)17 cells. Both CD4(+) T(H) subsets are highly susceptible to lysis by NK cells after activation. Administration of antibody that activates NK cells through blockade of its inhibitory CD94/NKG2A receptor allows enhanced elimination of pathogenic follicular T(H) and T(H)17 cells and arrest of disease progression. These results suggest that antibody-dependent enhancement of NK activity may yield effective, previously undescribed therapeutic approaches to this autoimmune disorder.
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Wang, Xiaoyang,1965Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology(Swepub:gu)xwanxi
(author)
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Wenander, Carola Schellack
(author)
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Spee, Pieter
(author)
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Cantor, Harvey
(author)
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Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för fysiologi
(creator_code:org_t)
Related titles
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In:Proceedings of the National Academy of Sciences of the United States of America: Proceedings of the National Academy of Sciences108:35, s. 14584-91091-6490
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In:Proceedings of the National Academy of Sciences: Proceedings of the National Academy of Sciences108:35, s. 14584-90027-8424
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