Due to the clinical and pathological similarities of EAE and MS, EAE has been used as a model for the study of human demyelinating disease. Both EAE and MS are characterized by a relapsing-remitting disease course with subsequent progressive disability. EAE is characterized by chronic inflammatory demyelination of the central nervous system (CNS) and involves autoimmune CD4+ Th1 cells. These cells develop in the peripheral lymphoid organ and travel to the CNS causing an immune response. The development of T cells is controlled largely by the expression of various cytokines as well as cellular adhesion molecules.
Pathology of MS
The pathology of MS starts with the activation and proliferation of T cells in the peripheral lymphoid organs. MMPs and adhesion molescules assist the T cells in crossing the blood brain barrier where the T cell engages antigen-MHC complexes in the CNS causing nerve cell damage.
MD Biosciences offers pre clinical contract research services for the following EAE models:
| EAE Model |
Description |
Length |
Strain |
| MBP-induced EAE |
self-limiting EAE model involving infiltration of T cells and inflammation around the spinal cord |
21 days |
Lewis rats |
| MOG-induced EAE |
chronic EAE model involving damage to the myelin and infiltration of T cells to spinal cord |
35 days |
C57BL/6 |
| Relapsing PLP-induced EAE |
relapsing EAE model with damage to the myelin and infiltration of T cells to spinal cord. First disease peak occurs between days 18-21 and second disease peak occurs around day 30 |
25-49 days |
SJL mice |