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Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
Published on: March 26, 2019
Targeting the tetraspanin CD81 blocks monocyte transmigration and ameliorates EAE
S Dijkstra1, G Kooij, R Verbeek
1Department of Molecular Cell Biology and Immunology, VU University Medical Center, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands. s.dijkstra@vumc.nl
Neurobiology of Disease
|July 1, 2008
Summary
Blocking CD81, a molecule involved in cell interactions, can reduce inflammation and neurological symptoms in multiple sclerosis (MS) models. This suggests CD81 as a potential therapeutic target for MS treatment.
Area of Science:
- Neuroimmunology
- Cellular and Molecular Immunology
Background:
- Leukocyte infiltration is crucial in multiple sclerosis (MS) demyelinating lesions.
- Targeting leukocyte-endothelial interactions offers therapeutic potential for MS.
Purpose of the Study:
- To investigate the therapeutic potential of blocking CD81 in multiple sclerosis (MS) models.
- To evaluate the effects of CD81 blockade on leukocyte transmigration and experimental autoimmune encephalomyelitis (EAE).
Main Methods:
- Utilized in vitro models with rodent and human brain endothelial cells to assess monocyte transmigration.
- Administered anti-CD81 monoclonal antibodies (mAbs) in vivo to mice with experimental autoimmune encephalomyelitis (EAE).
Main Results:
- Anti-CD81 mAb significantly reduced monocyte transmigration across endothelial monolayers in vitro.
- Preventive treatment with Eat2 anti-CD81 mAb ameliorated neurological symptoms and reduced spinal cord inflammation in EAE mice.
Conclusions:
- CD81 plays a significant role in leukocyte infiltration in the context of MS.
- Targeting CD81 presents a promising therapeutic strategy for mitigating inflammatory neurological damage in MS.
