prikaz prve stranice dokumenta An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response
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Scientific paper - Original scientific paper
An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response
Nature Immunology, (2024); https://doi.org/10.1038/s41590-024-01848-3
Šestan, Marko; Mikašinović, Sanja; Benić, Ante; Wueest, Stephan; Dimitropoulos, Christoforos; Mladenić, Karlo; Krapić, Mia; Hiršl, Lea; Glantzspiegel, Yossef; Rasteiro, Ana; Aliseychik, Maria; Cekinović Grbeša, Đurđica; Turk Wensveen, Tamara; Babić, Marina; Gat-Viks, Irit; Veiga-Fernandes, Henrique; Konrad, Daniel; Wensveen, Felix M.; Polić, Bojan More authors...

Cite this document

Šestan, M., Mikašinović, S., Benić, A., Wueest, S., Dimitropoulos, C., Mladenić, K. ... Polić, B. (2024). An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response. Nature Immunology. doi: 10.1038/s41590-024-01848-3

Šestan, Marko, et al. "An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response." Nature Immunology, 2024. https://doi.org/10.1038/s41590-024-01848-3

Šestan, Marko, Sanja Mikašinović, Ante Benić, Stephan Wueest, Christoforos Dimitropoulos, Karlo Mladenić, Mia Krapić, et al. "An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response." Nature Immunology (2024). https://doi.org/10.1038/s41590-024-01848-3

Šestan, M., et al. (2024) 'An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response', Nature Immunology. doi: 10.1038/s41590-024-01848-3

Šestan M, Mikašinović S, Benić A, Wueest S, Dimitropoulos C, Mladenić K, and sur.. An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response. Nature Immunology [Internet]. 2024 May 29 [cited 2024 November 14]. doi: 10.1038/s41590-024-01848-3

M. Šestan, et al., "An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response", Nature Immunology, May 2024. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:483038. [Accessed: 14 November 2024]

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Metadata
Title (english)An IFNγ-dependent immune–endocrine circuit lowers blood glucose to potentiate the innate antiviral immune response
AuthorMarko Šestan
AuthorSanja Mikašinović
AuthorAnte Benić
AuthorStephan Wueest
AuthorChristoforos Dimitropoulos
AuthorKarlo Mladenić
AuthorMia Krapić
AuthorLea Hiršl
AuthorYossef Glantzspiegel
AuthorAna Rasteiro
AuthorMaria Aliseychik
AuthorĐurđica Cekinović Grbeša
AuthorTamara Turk Wensveen
AuthorMarina Babić
AuthorIrit Gat-Viks
AuthorHenrique Veiga-Fernandes
AuthorDaniel Konrad
AuthorFelix M. Wensveen
AuthorBojan Polić
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Center for Proteomics)
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Histology and Embryology)
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Molecular Medicine and Biotechnology)
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Infectious Diseases)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
Viral infection makes us feel sick as the immune system alters systemic metabolism to better fight the pathogen. The extent of these changes is relative to the severity of disease. Whether blood glucose is subject to infection-induced modulation is mostly unknown. Here we show that strong, nonlethal infection restricts systemic glucose availability, which promotes the antiviral type I interferon (IFN-I) response. Following viral infection, we find that IFNγ produced by γδ T cells stimulates pancreatic β cells to increase glucose-induced insulin release. Subsequently, hyperinsulinemia lessens hepatic glucose output. Glucose restriction enhances IFN-I production by curtailing lactate-mediated inhibition of IRF3 and NF-κB signaling. Induced hyperglycemia constrained IFN-I production and increased mortality upon infection. Our findings identify glucose restriction as a physiological mechanism to bring the body into a heightened state of responsiveness to viral pathogens. This immune–endocrine circuit is disrupted in hyperglycemia, possibly explaining why patients with diabetes are more susceptible to viral infection.
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusAccepted
Peer reviewPeer review - international
Publication versionPublished version
Journal titleNature Immunology
p-ISSN1529-2908
e-ISSN1529-2916
DOIhttps://doi.org/10.1038/s41590-024-01848-3
URN:NBNurn:nbn:hr:184:483038
Publication2024-05-29
ProjectNumber: IP-2016-06-9306
Title (croatian): Imunosni mehanizmi u razvoju upale i metaboličkog sindroma u debljini
Title (english): Immune mechanisms in development of inflammation and metabolic syndrome in obesity
Acronym: INFLAMETAB
Leader: Bojan Polić
Jurisdiction: Croatia
Funding stream: Research Projects
ProjectNumber: IP-2020-02-7928
Title (croatian): Utjecaj šećerne bolesti tipa 2 i njezinog liječenja na funkciju limfocita
Title (english): Utjecaj šećerne bolesti tipa 2 i njezinog liječenja na funkciju limfocita
Acronym: DIABOLYC
Leader: Tamara Turk Wensveen
Jurisdiction: Croatia
Funding stream: Research Projects
ProjectNumber: KK.01.1.1.01.0006
Title (croatian): Jačanje kapaciteta CERVIRVAC-a za istraživanja u virusnoj imunologiji i vakcinologiji
Title (english): Strengthening the capacity of CerVirVac (Croatian Centre of Excellence for Virus Immunology and Vaccines) for research in viral immunology and vaccinology
Leader: Stipan Jonjić
Jurisdiction: eu
Funding stream: European Regional Development Fund
Document URLhttps://www.nature.com/articles/s41590-024-01848-3
Type of resourceText
Access conditionsClosed access
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Created on2024-05-31 06:26:07