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The Journal of Immunology, 2005, 174: 767-776.
Copyright © 2005 by The American Association of Immunologists

Dendritic Cells and NK Cells Stimulate Bystander T Cell Activation in Response to TLR Agonists through Secretion of IFN-{alpha}{beta} and IFN-{gamma}1

Arun T. Kamath, Christopher E. Sheasby and David F. Tough2

The Edward Jenner Institute for Vaccine Research, Compton, Newbury, United Kingdom

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-{alpha}{beta}, secreted by dendritic cells (DCs), and IFN-{gamma}, secreted by NK cells; notably, IFN-{gamma}-secreting NK cells expressed CD11c and copurified with DCs. Production of IFN-{gamma} 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-{gamma}, maximal IFN-{gamma} production required both direct contact of NK cells with DCs and DC-secreted cytokines. In vitro, IFN-{alpha}{beta}, IL-18, and IL-12 all contributed to DC stimulation of NK cell IFN-{gamma}, whereas IFN-{alpha}{beta} was shown to be important for induction of T cell bystander activation and NK cell IFN-{gamma} production in vivo. The results delineate a pathway involving innate immune mediators through which TLR agonists trigger bystander activation of T cells.




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