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AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity

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AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity. / Schmid, E.T.; Pang, I.K.; Carrera Silva, E.A.; Bosurgi, L.; Miner, J.J.; Diamond, M.S.; Iwasaki, A.; Rothlin, C.V.

in: ELIFE, Jahrgang 5, 2016, S. e12414.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Schmid, ET, Pang, IK, Carrera Silva, EA, Bosurgi, L, Miner, JJ, Diamond, MS, Iwasaki, A & Rothlin, CV 2016, 'AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity', ELIFE, Jg. 5, S. e12414. https://doi.org/10.7554/eLife.12414.001

APA

Schmid, E. T., Pang, I. K., Carrera Silva, E. A., Bosurgi, L., Miner, J. J., Diamond, M. S., Iwasaki, A., & Rothlin, C. V. (2016). AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity. ELIFE, 5, e12414. https://doi.org/10.7554/eLife.12414.001

Vancouver

Schmid ET, Pang IK, Carrera Silva EA, Bosurgi L, Miner JJ, Diamond MS et al. AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity. ELIFE. 2016;5:e12414. https://doi.org/10.7554/eLife.12414.001

Bibtex

@article{a9bfcadfa5bd4961ad29895743c05d61,
title = "AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity",
abstract = "The receptor tyrosine kinase (RTK) AXL is induced in response to type I interferons (IFNs) and limits their production through a negative feedback loop. Enhanced production of type I IFNs in Axl(-/-) dendritic cells (DCs) in vitro have led to speculation that inhibition of AXL would promote antiviral responses. Notwithstanding, type I IFNs also exert potent immunosuppressive functions. Here we demonstrate that ablation of AXL enhances the susceptibility to infection by influenza A virus and West Nile virus. The increased type I IFN response in Axl(-/-) mice was associated with diminished DC maturation, reduced production of IL-1β, and defective antiviral T cell immunity. Blockade of type I IFN receptor or administration of IL-1β to Axl(-/-) mice restored the antiviral adaptive response and control of infection. Our results demonstrate that AXL is essential for limiting the immunosuppressive effects of type I IFNs and enabling the induction of protective antiviral adaptive immunity.",
author = "E.T. Schmid and I.K. Pang and {Carrera Silva}, E.A. and L. Bosurgi and J.J. Miner and M.S. Diamond and A. Iwasaki and C.V. Rothlin",
year = "2016",
doi = "10.7554/eLife.12414.001",
language = "English",
volume = "5",
pages = "e12414",
journal = "ELIFE",
issn = "2050-084X",
publisher = "eLife Sciences Publications",

}

RIS

TY - JOUR

T1 - AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity

AU - Schmid, E.T.

AU - Pang, I.K.

AU - Carrera Silva, E.A.

AU - Bosurgi, L.

AU - Miner, J.J.

AU - Diamond, M.S.

AU - Iwasaki, A.

AU - Rothlin, C.V.

PY - 2016

Y1 - 2016

N2 - The receptor tyrosine kinase (RTK) AXL is induced in response to type I interferons (IFNs) and limits their production through a negative feedback loop. Enhanced production of type I IFNs in Axl(-/-) dendritic cells (DCs) in vitro have led to speculation that inhibition of AXL would promote antiviral responses. Notwithstanding, type I IFNs also exert potent immunosuppressive functions. Here we demonstrate that ablation of AXL enhances the susceptibility to infection by influenza A virus and West Nile virus. The increased type I IFN response in Axl(-/-) mice was associated with diminished DC maturation, reduced production of IL-1β, and defective antiviral T cell immunity. Blockade of type I IFN receptor or administration of IL-1β to Axl(-/-) mice restored the antiviral adaptive response and control of infection. Our results demonstrate that AXL is essential for limiting the immunosuppressive effects of type I IFNs and enabling the induction of protective antiviral adaptive immunity.

AB - The receptor tyrosine kinase (RTK) AXL is induced in response to type I interferons (IFNs) and limits their production through a negative feedback loop. Enhanced production of type I IFNs in Axl(-/-) dendritic cells (DCs) in vitro have led to speculation that inhibition of AXL would promote antiviral responses. Notwithstanding, type I IFNs also exert potent immunosuppressive functions. Here we demonstrate that ablation of AXL enhances the susceptibility to infection by influenza A virus and West Nile virus. The increased type I IFN response in Axl(-/-) mice was associated with diminished DC maturation, reduced production of IL-1β, and defective antiviral T cell immunity. Blockade of type I IFN receptor or administration of IL-1β to Axl(-/-) mice restored the antiviral adaptive response and control of infection. Our results demonstrate that AXL is essential for limiting the immunosuppressive effects of type I IFNs and enabling the induction of protective antiviral adaptive immunity.

UR - http://www.scopus.com/inward/record.url?eid=2-s2.0-84978880909&partnerID=MN8TOARS

U2 - 10.7554/eLife.12414.001

DO - 10.7554/eLife.12414.001

M3 - SCORING: Journal article

C2 - 27350258

VL - 5

SP - e12414

JO - ELIFE

JF - ELIFE

SN - 2050-084X

ER -