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Published on: August 11, 2014
Targeting antigen to diverse APCs inactivates memory CD8+ T cells without eliciting tissue-destructive effector
Tony J Kenna1, Tanya Waldie, Alice McNally
1Diamantina Institute for Cancer, Immunology and Metabolic Medicine, University of Queensland, Brisbane, Australia.
Journal of Immunology (Baltimore, Md. : 1950)
|December 10, 2009
Summary
Targeting antigens to MHC class II+ antigen-presenting cells (APCs) rapidly inactivates memory CD8+ T cells. This approach prevents tissue destruction and offers a new strategy for treating autoimmune diseases.
Area of Science:
- Immunology
- Autoimmune Diseases
- T cell biology
Background:
- Memory T cells emerge early in autoimmune diseases and resist tolerance induction.
- These cells pose a significant challenge to effective immunotherapy for established autoimmune conditions.
- Previous strategies targeting antigen to dendritic cells showed slow inactivation of memory CD8+ T cells, allowing tissue damage.
Purpose of the Study:
- To compare different antigen-targeting strategies for inactivating memory CD8+ T cells.
- To investigate the efficacy of MHC class II promoter-driven antigen expression in various antigen-presenting cells (APCs).
- To determine if rapid inactivation of memory CD8+ T cells can prevent tissue-destructive effector functions.
Main Methods:
- Utilized an MHC class II promoter to drive antigen expression in a diverse array of APCs.
- Compared antigen-targeting strategies for their ability to inactivate CD8+ memory T cells.
- Analyzed the mechanism of inactivation, focusing on T cell receptor (TCR) downregulation.
Main Results:
- Targeting antigen to MHC class II+ hematopoietic APCs led to rapid inactivation of CD8+ memory T cells.
- This inactivation involved swift and sustained downregulation of the TCR.
- The effector response of CD8+ memory cells was effectively truncated, preventing target tissue destruction.
Conclusions:
- Genetically targeting antigens to a broad range of MHC class II+ APCs is a highly efficient method for terminating memory CD8+ T cell responses.
- This strategy effectively prevents tissue-destructive effector functions mediated by these cells.
- This approach holds promise for preventing and treating established autoimmune diseases.
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