Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2014 Jun 20;5:308. doi: 10.3389/fmicb.2014.00308

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2014 Münz.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Plasmacytoid, conventional and monocyte-derived DCs might contribute to EBV specific immune control. Unmethylated DNA of EBV particles and EBERs of EBV-infected B cells (LCLs) mature plasmacytoid (pDCs) and conventional or monocyte-derived DCs (cDCs or moDCs) via TLR9 or TLR3 stimulation, respectively. These mature pDC and cDC or moDC populations activate natural killer (NK) and T cells via type I interferon (IFNα/β) or interleukin 12 (IL-12) secretion, respectively. For T-cell stimulation by MHC presentation they acquire EBV antigens either via phagocytosis of dying LCLs (for cDCs and moDCs) or trogocytosis of EBV epitope presenting MHC complexes (pDCs). The activated NK and primed T cells then delay primary EBV infection via IFNγ and kill infected cells. PDCs can also delay primary EBV infection via IFNα/β production.