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Purification of the Membrane Compartment for Endoplasmic Reticulum-associated Degradation of Exogenous Antigens in Cross-presentation
Published on: August 21, 2017
Development of antigen cross-presentation capacity in dendritic cells
Christiane Dresch1, Yann Leverrier, Jacqueline Marvel
1Institute of Virology, University of Zurich, Zurich 8057, Switzerland.
Trends in Immunology
|June 9, 2012
Summary
Dendritic cells (DCs) present external antigens via MHC class I, crucial for immunity and self-tolerance. This cross-presentation ability develops in CD8+ DCs during inflammation, but is innate in thymic CD8+ DCs for deleting self-reactive T cells.
Area of Science:
- Immunology
- Cell Biology
Background:
- Cross-presentation of exogenous antigens by dendritic cells (DCs) on MHC class I molecules is critical for initiating adaptive immune responses against intracellular pathogens and for establishing self-tolerance.
- The CD8+ DC lineage in mice is specialized for this cross-presentation function.
Purpose of the Study:
- To investigate the developmental regulation of cross-presentation capacity in CD8+ dendritic cells.
- To understand the differences in cross-presentation ability between peripheral and thymic CD8+ DCs.
Main Methods:
- Analysis of cross-presentation capacity in different DC subsets.
- Investigating the role of cytokines like granulocyte macrophage colony-stimulating factor (GM-CSF) and toll-like receptor (TLR) ligands in inducing cross-presentation.
Main Results:
- CD8+ DCs do not inherently possess cross-presentation capacity at birth; it is acquired during later developmental stages.
- Inflammation or infection, signaled by GM-CSF or TLR ligands, induces cross-presentation in peripheral CD8+ DCs.
- Steady-state thymic CD8+ DCs exhibit fully developed cross-presentation capacity, independent of inflammatory signals.
Conclusions:
- Cross-presentation capacity in CD8+ DCs is developmentally regulated and context-dependent.
- The innate cross-presentation ability of thymic CD8+ DCs supports their role in central T cell tolerance by deleting self-reactive T cells.
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