prikaz prve stranice dokumenta NK cells link obesity-induced adipose stress to inflammation and insulin resistance
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Scientific paper - Original scientific paper
NK cells link obesity-induced adipose stress to inflammation and insulin resistance
Nature Immunology, 16 (2015), 4; 376-385. https://doi.org/10.1038/ni.3120
Wensveen, Felix M; Jelenčić, Vedrana; Valentić, Sonja; Šestan, Marko; Wensveen, Tamara Turk; Theurich, Sebastian; Glasner, Ariella; Mendrila, Davor; Štimac, Davor; Wunderlich, F Thomas; Brüning, Jens C; Mandelboim, Ofer; Polić, Bojan

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Cite this document

Wensveen, F. M., Jelenčić, V., Valentić, S., Šestan, M., Wensveen, T. T., Theurich, S. ... Polić, B. (2015). NK cells link obesity-induced adipose stress to inflammation and insulin resistance. Nature Immunology, 16. (4), 376-385. doi: 10.1038/ni.3120

Wensveen, Felix M, et al. "NK cells link obesity-induced adipose stress to inflammation and insulin resistance." Nature Immunology, vol. 16, no. 4, 2015, pp. 376-385. https://doi.org/10.1038/ni.3120

Wensveen, Felix M, Vedrana Jelenčić, Sonja Valentić, Marko Šestan, Tamara Turk Wensveen, Sebastian Theurich, Ariella Glasner, et al. "NK cells link obesity-induced adipose stress to inflammation and insulin resistance." Nature Immunology 16, no. 4 (2015): 376-385. https://doi.org/10.1038/ni.3120

Wensveen, F. M., et al. (2015) 'NK cells link obesity-induced adipose stress to inflammation and insulin resistance', Nature Immunology, 16(4), pp. 376-385. doi: 10.1038/ni.3120

Wensveen FM, Jelenčić V, Valentić S, Šestan M, Wensveen TT, Theurich S, and sur.. NK cells link obesity-induced adipose stress to inflammation and insulin resistance. Nature Immunology [Internet]. 2015 March 02 [cited 2024 May 05];16(4):376-385. doi: 10.1038/ni.3120

F. M. Wensveen, et al., "NK cells link obesity-induced adipose stress to inflammation and insulin resistance", Nature Immunology, vol. 16, no. 4, pp. 376-385, March 2015. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:907823. [Accessed: 05 May 2024]

Metadata
Title (english)NK cells link obesity-induced adipose stress to inflammation and insulin resistance
AuthorFelix M Wensveen
AuthorVedrana Jelenčić
AuthorSonja Valentić
AuthorMarko Šestan
AuthorTamara Turk Wensveen
AuthorSebastian Theurich
AuthorAriella Glasner
AuthorDavor Mendrila
AuthorDavor Štimac
AuthorF Thomas Wunderlich
AuthorJens C Brüning
AuthorOfer Mandelboim
AuthorBojan Polić
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Histology and Embryology)
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Internal Medicine)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
An important cause of obesity-induced insulin resistance is chronic systemic inflammation originating in visceral adipose tissue (VAT). VAT inflammation is associated with the accumulation of proinflammatory macrophages in adipose tissue, but the immunological signals that trigger their accumulation remain unknown. We found that a phenotypically distinct population of tissue-resident natural killer (NK) cells represented a crucial link between obesity-induced adipose stress and VAT inflammation. Obesity drove the upregulation of ligands of the NK cell-activating receptor NCR1 on adipocytes; this stimulated NK cell proliferation and interferon-gamma (IFN-gamma) production, which in turn triggered the differentiation of proinflammatory macrophages and promoted insulin resistance. Deficiency of NK cells, NCR1 or IFN-gamma prevented the accumulation of proinflammatory macrophages in VAT and greatly ameliorated insulin sensitivity. Thus NK cells are key regulators of macrophage polarization and insulin resistance in response to obesity-induced adipocyte stress.
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleNature Immunology
Numberingvol. 16, no. 4, pp. 376-385
p-ISSN1529-2908
e-ISSN1529-2916
DOIhttps://doi.org/10.1038/ni.3120
URN:NBNurn:nbn:hr:184:907823
Publication2015-03-02
Publication2015-04
Document URLhttp://www.nature.com/articles/ni.3120
Type of resourceText
Access conditionsRestricted access
Terms of useLicence In copyright icon
Created on2018-11-05 10:57:56