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Published on: October 18, 2016
Impact of human myelin on the maturation and function of human monocyte-derived dendritic cells
Viktoria Gredler1, Susanne Ebner, Kathrin Schanda
1Clinical Department of Neurology, Innsbruck Medical University, Austria.
Insights
Human myelin impairs the activation of dendritic cells (DC), affecting their ability to stimulate T cells. This suggests myelin plays a key role in balancing immune responses and tolerance in multiple sclerosis.
Area of Science:
- Immunology
- Neuroscience
Background:
- Macrophages and dendritic cells (DCs) are crucial in multiple sclerosis (MS) immunopathology.
- Understanding how myelin impacts DC function is vital for MS research.
Purpose of the Study:
- To investigate the effect of human myelin on monocyte-derived dendritic cells (moDCs).
- To characterize the immunostimulatory capacity and T cell-biasing potential of myelin-exposed moDCs.
Main Methods:
- moDCs were cultured with human myelin and stimulated with LPS or a maturation cocktail.
- DC activation was assessed via cell surface marker expression and cytokine/chemokine secretion.
- Immunostimulatory capacity was evaluated using allogeneic mixed-leukocyte reactions (MLRs) and T cell differentiation assays (Th1, Th17, Treg).
Main Results:
- Phagocytosis of myelin by moDCs impaired their activation and reduced their ability to stimulate allogeneic T cells.
- Myelin exposure led to increased TGF-beta1 production and diminished CCR7 upregulation in moDCs.
- Myelin did not significantly affect the differentiation of T helper cell subsets (Th1, Th17, Treg).
Conclusions:
- Myelin significantly influences dendritic cell activation, potentially impairing immune responses in MS.
- Myelin's impact on DC function suggests a critical role in modulating the balance between immunity and tolerance in the central nervous system.
Abstract:
Macrophages and dendritic cells (DC) play an important role in the immunopathology of multiple sclerosis. We analyzed the impact of human myelin on monocyte-derived DC and describe their immunostimulatory capacity. Cells were grown on myelin and stimulated with LPS or a defined maturation cocktail. DC activation was analyzed by the expression of cell surface markers and the secretion of cytokines and chemokines. The immunostimulatory capacity of DC was assessed by allogeneic mixed-leukocyte reactions via proliferation. Additionally, their ability to bias T cells towards Th1, Th17 or Treg differentiation was investigated. We found that phagocytosis of myelin impaired the activation of DC, displayed by an impaired ability to stimulate allogeneic T cells, an increased production of TGF-beta1 and a diminished upregulation of CCR7 but did not affect the differentiation into T helper cell subsets. We hypothesize that myelin influences DC activation and plays a pivotal role in balancing immunity and tolerance.
