Spinal Cord Homogenate Induced EAE
SCH-induced EAE is induced in DA rats with a homogenate of spinal cord from naive animals emulsified in Incomplete Freunds Adjuvant (IFA). SCH-induced EAE is a severe, relapsing and demyelinating encephalomyelitis. Animals with EAE develop ascending flaccid paralysis that initially affects the tail (score 1-2), later involves hind limbs (score 3-6), forelimbs (score 7) and ultimately result in quadriplegia and death (score 8). The disease is CD4+ T cell mediated and dependent on both Th1 and Th17 cells.
In this model, disease is accompanied by demyelination of the CNS as can be assessed by histology at termination. In additon, IL-17 and IFN-g responses from LNs cells can be assayed ex vivo either as estimation on drug efficacy in vitro or prediction of efficacy for selection of lead compounds before in vivo experiments. The CD4+ T cell dependency of this model allows for adoptive T cell transfer following ex vivo stimulation of autoreactive T cells.
MOG1-125 induced EAE
MOG-induced EAE is induced in DA or Lewis rats with protein emulsified in Incomplete Freunds Adjuvant (IFA) or Complete Freunds Adjuvant (CFA) respectively, and are models well suited for studies of immune mechanisms relevant to MS. MOG-induced EAE is a severe and demyelinating encephalomyelitis with a chronic progressive disease course. The disease is CD4+ T cell mediated and dependent on both Th1 and Th17 cells. T cells, B cells and macrophages are recruited to the inflammatory site resulting in demyelination and axonal loss. IL-17 and IFN-g responses from LNs cells can be assayed ex vivo as estimation on drug efficacy in vivo or prediction of efficacy for selection of lead compounds before in vivo experiments. The CD4+ T cell dependency of this model allows for adoptive T cell transfer following ex vivo stimulation of autoreactive T cells.
MBP induced EAE
MBP-induced EAE is induced in Lewis rats with MBP protein emulsified in Complete Freunds Adjuvant (CFA). MBP-induced EAE is a severe encephalomyelitis with an acute monophasic disease course. Disease has an onset around day 8-10 after immunization and experiment can normally be terminated around day 20. In this model, disease is not accompanied by demyelination of the CNS and there is mainly infiltration of T cells in the CNS. The model is thus suitable for studies to assess basic immunological mechanisms in regard to T cell function in autoimmune disease.