Herpes Simplex Virus Induces the Early Activation of NK Cell via MyD88- Dependent Signal
Stacie N. Woolard1, Divya G. Venkat1, Evelyn Kurt Jones2, Uday Kumaraguru*, 1
Identifiers and Pagination:Year: 2010
First Page: 36
Last Page: 44
Publisher Id: TOIJ-3-36
Article History:Received Date: 24/12/2009
Revision Received Date: 1/5/2010
Acceptance Date: 14/5/2010
Electronic publication date: 22/6/2010
Collection year: 2010
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In the course of a Herpes Simples Virus type-1 (HSV-1) infection, the bidirectional cross-talk between Natural Killer (NK) cells and Dendritic Cells (DCs) is imperative in mounting an efficient immunological response. Enhanced DC maturation by Toll-Like Receptor (TLR) ligands is considered as a pivotal link between innate and adaptive immune responses, yet the impact of direct TLR signaling on NK:DC interaction during an HSV infection has yet to be examined. We demonstrate that HSV mediates the activation of NK cells and the induction of the cooperative relationship between NK cells and DCs via TLR. During the course of an HSV infection, the initial response required both types of innate cells and demonstrated phenotypic and functional activation much like that of TLR-stimulated cells. Using a MyD88 knock-out system diminished the early interaction between DCs and NK after HSV exposure. Our results indicate that HSV TLRligands modulate the early NK: DC interaction and may be a mechanism used by these innate immune cells to overcome virus mediated immune evasion and the initiation of a potent acquired immune response.