NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells

Babić, Marina; Dimitropoulos, Christoforos; Hammer, Quirin; Stehle, Christina; Heinrich, Frederik; Sarsenbayeva, Assel; Eisele, Almut; Durek, Pawel; Mashreghi, Mir-Farzin; Lisnić, Berislav; Van Snick, Jacques; Löhning, Max; Fillatreau, Simon; Withers, David R.; Gagliani, Nicola; Huber, Samuel; Flavell, Richard A.; Polić, Bojan; Romagnani, Chiara

doi:10.1084/jem.20190133

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Scientific paper - Original scientific paper

NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells

Journal of Experimental Medicine, 217 (2020), 8; e20190133. https://doi.org/10.1084/jem.20190133

Babić, Marina; Dimitropoulos, Christoforos; Hammer, Quirin; Stehle, Christina; Heinrich, Frederik; Sarsenbayeva, Assel; Eisele, Almut; Durek, Pawel; Mashreghi, Mir-Farzin; Lisnić, Berislav; Van Snick, Jacques; Löhning, Max; Fillatreau, Simon; Withers, David R.; Gagliani, Nicola; Huber, Samuel; Flavell, Richard A.; Polić, Bojan; Romagnani, Chiara More authors...

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APA 6th Edition

Babić, M., Dimitropoulos, C., Hammer, Q., Stehle, C., Heinrich, F., Sarsenbayeva, A. ... Romagnani, C. (2020). NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells. Journal of Experimental Medicine, 217. (8). doi: 10.1084/jem.20190133

MLA 8th Edition

Babić, Marina, et al. "NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells." Journal of Experimental Medicine, vol. 217, no. 8, 2020. https://doi.org/10.1084/jem.20190133

Chicago 17th Edition

Babić, Marina, Christoforos Dimitropoulos, Quirin Hammer, Christina Stehle, Frederik Heinrich, Assel Sarsenbayeva, Almut Eisele, et al. "NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells." Journal of Experimental Medicine 217, no. 8 (2020). https://doi.org/10.1084/jem.20190133

Harvard

Babić, M., et al. (2020) 'NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells', Journal of Experimental Medicine, 217(8). doi: 10.1084/jem.20190133

Vancouver

Babić M, Dimitropoulos C, Hammer Q, Stehle C, Heinrich F, Sarsenbayeva A, and sur.. NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells. Journal of Experimental Medicine [Internet]. 2020 August 03 [cited 2024 November 24];217(8). doi: 10.1084/jem.20190133

IEEE

M. Babić, et al., "NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells", Journal of Experimental Medicine, vol. 217, no. 8, August 2020. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:299388. [Accessed: 24 November 2024]

Cite this item: https://urn.nsk.hr/urn:nbn:hr:184:299388

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Metadata

Title (english)	NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells
Author	Marina Babić
Author	Christoforos Dimitropoulos
Author	Quirin Hammer
Author	Christina Stehle
Author	Frederik Heinrich
Author	Assel Sarsenbayeva
Author	Almut Eisele
Author	Pawel Durek
Author	Mir-Farzin Mashreghi
Author	Berislav Lisnić
Author	Jacques Van Snick
Author	Max Löhning
Author	Simon Fillatreau
Author	David R. Withers
Author	Nicola Gagliani
Author	Samuel Huber
Author	Richard A. Flavell
Author	Bojan Polić
Author	Chiara Romagnani
Author's institution	University of Rijeka Faculty of Medicine (Center for Proteomics)
Author's institution	University of Rijeka Faculty of Medicine (Department of Histology and Embryology)
Scientific / art field, discipline and subdiscipline	BIOMEDICINE AND HEALTHCARE Basic Medical Sciences
Abstract (english)	NKG2D is a danger sensor expressed on different subsets of innate and adaptive lymphocytes. Despite its established role as a potent activator of the immune system, NKG2D-driven regulation of CD4+ T helper (Th) cell–mediated immunity remains unclear. In this study, we demonstrate that NKG2D modulates Th1 and proinflammatory T-bet+ Th17 cell effector functions in vitro and in vivo. In particular, NKG2D promotes higher production of proinflammatory cytokines by Th1 and T-bet+ Th17 cells and reinforces their transcription of type 1 signature genes, including Tbx21. Conditional deletion of NKG2D in T cells impairs the ability of antigen-specific CD4+ T cells to promote inflammation in vivo during antigen-induced arthritis and experimental autoimmune encephalomyelitis, indicating that NKG2D is an important target for the amelioration of Th1- and Th17-mediated chronic inflammatory diseases.
Keywords (english)
Language	english
Publication type	Scientific paper - Original scientific paper
Publication status	Published
Peer review	Peer review - international
Publication version	Published version
Journal title	Journal of Experimental Medicine
Numbering	vol. 217, no. 8, e20190133
p-ISSN	0022-1007
e-ISSN	1540-9538
DOI	https://doi.org/10.1084/jem.20190133
URN:NBN	urn:nbn:hr:184:299388
Publication	2020-08-03
Project	Number: IP-2016-06-9306 Title (croatian): Imunosni mehanizmi u razvoju upale i metaboličkog sindroma u debljini Acronym: INFLAMETAB Leader: Bojan Polić Jurisdiction: Croatia Funding stream: IP
Document URL	https://rupress.org/jem/article/doi/10.1084/jem.20190133/151818/NK-cell-receptor-NKG2D-enforces-proinflammatory
Type of resource	Text
Access conditions	Open access
Terms of use
Created on	2021-03-09 09:51:51