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Published on: May 21, 2012
Dendritic cells maximize the memory CD8 T cell response to infection
David J Zammit1, Linda S Cauley, Quynh-Mai Pham
1Division of Immunology, University of Connecticut Health Center, Farmington, CT 06030, USA.
Insights
Dendritic cells (DCs) are crucial for reactivating memory CD8 T cells during infections. Their interaction is a major mechanism driving T cell reactivation in vivo, even in tissue-specific infections.
Area of Science:
- Immunology
- Cellular Biology
- Infectious Diseases
Background:
- Costimulatory signals from dendritic cells (DCs) are essential for naive T cell activation.
- The role of DCs in reactivating memory T cells during recall responses remains largely unknown.
Purpose of the Study:
- To investigate the extent to which dendritic cells (DCs) reactivate memory CD8 T cells during recall responses to microbial infections.
Main Methods:
- Utilized an in vivo depletion system to analyze DC function.
- Examined recall responses to vesicular stomatitis virus, Listeria monocytogenes, and influenza virus infections.
Main Results:
- A significant decrease in responding memory CD8 T cells was observed in lymphoid and nonlymphoid tissues.
- This reduction occurred during recall responses to all three tested microbial infections.
Conclusions:
- Dendritic cell interaction is a primary mechanism for T cell reactivation in vivo.
- This mechanism is important even in tissue-specific infections, such as those affecting the respiratory tract.
Abstract:
Costimulatory signals from dendritic cells (DCs) are required for naive T cells to respond to antigenic stimulation. To what extent DCs reactivate memory T cells during recall responses is not known. Here, an in vivo depletion system has been used to analyze the role of DCs in reactivating CD8 memory T cells during recall responses to three different microbial infections. We show a profound decrease in the numbers of responding memory CD8 T cells in both lymphoid and nonlymphoid tissues during the recall responses to infection with vesicular stomatitis virus, Listeria monocytogenes (Lm), or influenza virus. These data show that interaction with DCs is a major mechanism driving T cell reactivation in vivo, even during a tissue-specific infection of the respiratory tract.
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