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Distinct requirements for activation of NKT and NK cells during viral infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Qiao Verma, Shilpi Tyznik, Aaron J. Kronenberg, Mitchell Benedict, Chris A.
Description	Author Affiliation: Tyznik AJ ( Division of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037.)
Abstract	NK cells are key regulators of innate defense against mouse CMV (MCMV). Like NK cells, NKT cells also produce high levels of IFN-Î³ rapidly after MCMV infection. However, whether similar mechanisms govern activation of these two cell types, as well as the significance of NKT cells for host resistance, remain unknown. In this article, we show that, although both NKT and NK cells are activated via cytokines, their particular cytokine requirements differ significantly in vitro and in vivo. IL-12 is required for NKT cell activation in vitro but is not sufficient, whereas NK cells have the capacity to be activated more promiscuously in response to individual cytokines from innate cells. In line with these results, GM-CSF-derived dendritic cells activated only NK cells upon MCMV infection, consistent with their virtual lack of IL-12 production, whereas Flt3 ligand-derived dendritic cells produced IL-12 and activated both NK and NKT cells. In vivo, NKT cell activation was abolished in IL-12(-/-) mice infected with MCMV, whereas NK cells were still activated. In turn, splenic NK cell activation was more IL-18 dependent. The differential requirements for IL-12 and IL-18 correlated with the levels of cytokine receptor expression by NK and NKT cells. Finally, mice lacking NKT cells showed reduced control of MCMV, and depleting NK cells further enhanced viral replication. Taken together, our results show that NKT and NK cells have differing requirements for cytokine-mediated activation, and both can contribute nonredundantly to MCMV defense, revealing that these two innate lymphocyte subsets function together to fine-tune antiviral responses.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300837
Journal	The Journal of Immunology
Issue Number	8
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-04-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Killer Cells, Natural Immunology Lymphocyte Activation Natural Killer T-cells Virus Diseases Animals Cell Communication Cytokines Biosynthesis Pharmacology Dendritic Cells Metabolism Virology Gene Expression Immunity, Innate Interferon-gamma Interleukin-12 Drug Effects Mice Mice, Knockout Muromegalovirus Receptors, Cytokine Genetics Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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