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Dendritic Cells and NK Cells Stimulate Bystander T Cell Activation in Response to TLR Agonists through Secretion of IFN-αβ and IFN-γ

Content Provider	Scilit
Author	Kamath, Arun T. Sheasby, Christopher E. Tough, David F.
Copyright Year	2005
Description	Recognition of conserved features of infectious agents by innate pathogen receptors plays an important role in initiating the adaptive immune response. We have investigated early changes occurring among T cells after injection of TLR agonists into mice. Widespread, transient phenotypic activation of both naive and memory T cells was observed rapidly after injection of molecules acting through TLR3, -4, -7, and -9, but not TLR2. T cell activation was shown to be mediated by a combination of IFN-αβ, secreted by dendritic cells (DCs), and IFN-γ, secreted by NK cells; notably, IFN-γ-secreting NK cells expressed CD11c and copurified with DCs. Production of IFN-γ by NK cells could be stimulated by DCs from TLR agonist-injected mice, and although soluble factors secreted by LPS-stimulated DCs were sufficient to induce IFN-γ, maximal IFN-γ production required both direct contact of NK cells with DCs and DC-secreted cytokines. In vitro, IFN-αβ, IL-18, and IL-12 all contributed to DC stimulation of NK cell IFN-γ, whereas IFN-αβ was shown to be important for induction of T cell bystander activation and NK cell IFN-γ production in vivo. The results delineate a pathway involving innate immune mediators through which TLR agonists trigger bystander activation of T cells.
Ending Page	776
Page Count	10
Starting Page	767
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.174.2.767
Journal	The Journal of Immunology
Issue Number	2
Volume Number	174
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2005-01-15
Access Restriction	Open
Subject Keyword	Ifn Αβ Innate Immune Nk Cells Ifn Γ Cell Bystander
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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