Key result
In SJL mice with EAE, CNS-infiltrating cells showed a dominant response to the original disease-inducing epitope without evidence of determinant spread during relapse.
Population
SJL mice with experimental allergic encephalomyelitis (EAE)
Design
Preclinical
Follow-up
Tracked through acute disease, remission, and relapse
Authors
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Challenges determinant spread in EAE relapse; leaves open its role in human MS.
The study argues against a causal role for determinant spread in disease relapse in EAE models, showing instead a focused response to the original disease-inducing epitope.
Takács et al. (1997) studied Relapsing and remitting experimental allergic encephalomyelitis. Encephalitogenic proteolipid protein or myelin basic protein epitopes was evaluated on Determinant spread during relapsing and remitting EAE, correlating epitope recognition and cytokine production with disease severity. In SJL mice with EAE, CNS-infiltrating cells showed a dominant response to the original disease-inducing epitope without evidence of determinant spread during relapse.
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