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Published on: January 13, 2016
Apoptotic cell capture by DCs induces unexpectedly robust autologous CD4+ T-cell responses
Michael Valente1, Camille Baey, Pauline Louche
1Inserm U1016, Institut Cochin, Paris, France; CNRS UMR8104, Paris, France; University Paris Descartes, Paris, France.
Insights
Dendritic cells (DCs) engulfing apoptotic cells surprisingly activate naive CD4(+) T cells, leading to T-cell proliferation. These T cells can become suppressive or differentiate into IL-17-producing cells with a bacterial signal.
Area of Science:
- Immunology
- Cell Biology
Background:
- Apoptotic cells are typically linked to immune tolerance.
- Dendritic cells (DCs) engulf apoptotic cells as part of immune regulation.
Purpose of the Study:
- To investigate the immune response triggered by dendritic cells (DCs) loaded with apoptotic cells.
- To understand the role of apoptotic cell material in T-cell activation and differentiation.
Main Methods:
- Loading autologous DCs with autologous apoptotic cells.
- Analyzing CD4(+) T-cell proliferation and phenotype.
- Investigating the role of endo-lysosomal pathways and MHC class II presentation.
- Assessing T-cell suppressive capacity and IL-17 production in response to LPS stimulation.
Main Results:
- Autologous DCs loaded with apoptotic cells induced significant proliferation of naive CD4(+) T cells (>10% activation).
- Proliferation was dependent on endo-lysosomal processing and MHC class II presentation, not increased DC costimulation.
- Stimulated CD4(+) T cells showed suppressive capacities.
- In the presence of lipopolysaccharide (LPS), these DCs induced IL-17-producing cells.
Conclusions:
- DC engulfment of apoptotic cells can unexpectedly drive robust autologous CD4(+) T-cell responses.
- These responses initially generate suppressive CD4(+) T cells.
- A bacterial danger signal like LPS can redirect these cells towards a Th17 phenotype.
Abstract:
Apoptotic cells represent an important source of self-antigens and their engulfment by dendritic cells (DCs) is usually considered to be related to tolerance induction. We report here an unexpectedly high level of human CD4(+) T-cell proliferation induced by autologous DCs loaded with autologous apoptotic cells, due to the activation of more than 10% of naive CD4(+) T cells. This proliferation is not due to an increase in the costimulatory capacity of DCs, but is dependent on apoptotic cell-associated material processed through an endo-lysosomal pathway and presented on DC MHC class II molecules. Autologous CD4(+) T cells stimulated with apoptotic cell-loaded DCs exhibit suppressive capacities. However, in the presence of bacterial lipopolysaccharide, apoptotic cell-loaded DCs induce the generation of IL-17-producing cells. Thus, apoptotic cell engulfment by DCs may lead to increased autologous responses, initially generating CD4(+) T cells with suppressive capacities able to differentiate into Th17 cells in the presence of a bacterial danger signal such as LPS.
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