You are not currently logged in.
Access JSTOR through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Induction of Antiviral Immunity Requires Toll-Like Receptor Signaling in Both Stromal and Dendritic Cell Compartments
Ayuko Sato, Akiko Iwasaki and Ralph M. Steinman
Proceedings of the National Academy of Sciences of the United States of America
Vol. 101, No. 46 (Nov. 16, 2004), pp. 16274-16279
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3373808
Page Count: 6
You can always find the topics here!Topics: T lymphocytes, Human herpesvirus 2, Infections, Stromal cells, Viruses, Mice, Lymph nodes, Epithelial cells, Viral infections, Secretion
Were these topics helpful?See somethings inaccurate? Let us know!
Select the topics that are inaccurate.
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
Pattern recognition by Toll-like receptors (TLRs) is known to be important for the induction of dendritic cell (DC) maturation. DCs, in turn, are critically important in the initiation of T cell responses. However, most viruses do not infect DCs. This recognition system poses a biological problem in ensuring that most viral infections be detected by pattern recognition receptors. Furthermore, it is unknown what, if any, is the contribution of TLRs expressed by cells that are infected by a virus, versus TLRs expressed by DCs, in the initiation of antiviral adaptive immunity. Here we address these issues using a physiologically relevant model of mucosal infection with herpes simplex virus type 2. We demonstrate that innate immune recognition of viral infection occurs in two distinct stages, one at the level of the infected epithelial cells and the other at the level of the noninfected DCs. Importantly, both TLR-mediated recognition events are required for the induction of effector T cells. Our results demonstrate that virally infected tissues instruct DCs to initiate the appropriate class of effector T cell responses and reveal the critical importance of the stromal cells in detecting infectious agents through their own pattern recognition receptors.
Proceedings of the National Academy of Sciences of the United States of America © 2004 National Academy of Sciences