prikaz prve stranice dokumenta NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection
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Scientific paper - Original scientific paper
NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection
PLOS Pathogens, 15 (2019), 4; e1007725. https://doi.org/10.1371/journal.ppat.1007725
Pallmer, Katharina; Barnstorf, Isabel; Baumann, Nicolas S.; Borsa, Mariana; Jonjić, Stipan; Oxenius, Annette

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Pallmer, K., Barnstorf, I., Baumann, N. S., Borsa, M., Jonjić, S. & Oxenius, A. (2019). NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection. PLOS Pathogens, 15. (4). doi: 10.1371/journal.ppat.1007725

Pallmer, Katharina, et al. "NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection." PLOS Pathogens, vol. 15, no. 4, 2019. https://doi.org/10.1371/journal.ppat.1007725

Pallmer, Katharina, Isabel Barnstorf, Nicolas S. Baumann, Mariana Borsa, Stipan Jonjić and Annette Oxenius. "NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection." PLOS Pathogens 15, no. 4 (2019). https://doi.org/10.1371/journal.ppat.1007725

Pallmer, K., et al. (2019) 'NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection', PLOS Pathogens, 15(4). doi: 10.1371/journal.ppat.1007725

Pallmer K, Barnstorf I, Baumann NS, Borsa M, Jonjić S, Oxenius A. NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection. PLOS Pathogens [Internet]. 2019 April 17 [cited 2024 December 24];15(4). doi: 10.1371/journal.ppat.1007725

K. Pallmer, I. Barnstorf, N. S. Baumann, M. Borsa, S. Jonjić and A. Oxenius, "NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection", PLOS Pathogens, vol. 15, no. 4, April 2019. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:738160. [Accessed: 24 December 2024]

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Metadata
Title (english)NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection
AuthorKatharina Pallmer
AuthorIsabel Barnstorf
AuthorNicolas S. Baumann
AuthorMariana Borsa
AuthorStipan Jonjić
AuthorAnnette Oxenius
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Histology and Embryology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
Besides their function in recognizing cancerous and virally infected cells, natural killer (NK) cells have the potential to shape adaptive immune responses. However, the mechanisms employed by NK cells to negatively regulate virus-specific CD8 T cell responses remain to be fully defined. Using activating receptor natural cytotoxicity receptor (NCR) 1 deficient (NCR1gfp/gfp) mice, we found increased numbers of virus-specific CD8 T cells, leading to enhanced virus control during acute LCMV infection. Furthermore, virus-specific CD8 T cells were more activated in the absence of NCR1, resulting in exacerbated immunopathology, documented by weight loss, and superior virus control early during chronic LCMV infection. Transfer experiments of virus-specific CD8 T cells into NCR1 deficient hosts revealed a direct cross talk between NK and CD8 T cells. Studies on the splenic microarchitecture revealed pronounced disorganization of T cells in infected NCR1gfp/gfp mice, resulting in enhanced immunopathology and disruption of the T cell niche upon chronic LCMV infection. Our data show a novel pathway employed by NK cells to regulate antiviral CD8 T cell responses, namely direct recognition and elimination of activated CD8 T cells via NCR1 early during infection to protect the host from an overshooting T cell response.
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titlePLOS Pathogens
Numberingvol. 15, no. 4, e1007725
e-ISSN1553-7374
DOIhttps://doi.org/10.1371/journal.ppat.1007725
URN:NBNurn:nbn:hr:184:738160
Publication2019-04-17
Document URLhttp://dx.plos.org/10.1371/journal.ppat.1007725
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution 4.0 International (CC BY 4.0) icon
Created on2019-04-24 18:44:35