Animal model of autoimmune encephalomyelitis
Animal model of autoimmune encephalomyelitis
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Multiple sclerosis
Introduction to the EAE Animal Model
The experimental autoimmune encephalomyelitis (EAE) animal model is a classic experimental system for studying central nervous system autoimmune diseases such as multiple sclerosis. It is typically induced by immunizing animals with myelin‑related antigens—such as myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), or proteolipid protein (PLP)—in combination with complete Freund’s adjuvant. Following model induction, the peripheral immune system becomes activated and erroneously targets the myelin sheath of the central nervous system, leading to inflammatory cell infiltration, demyelination, and axonal damage. Consequently, affected animals progressively exhibit neurological deficits, including tail weakness, hindlimb paralysis, and impaired motor coordination. This model is widely employed to investigate the pathogenic mechanisms of autoimmune demyelinating disorders and to evaluate immunomodulatory therapeutics.
EAE Animal Model Platform Service Advantages of Aniphe BioLab
The EAE animal model platform developed by Ailinfei is centered on robust immune induction and the reproducible recapitulation of central demyelinating pathology, providing a reliable in vivo system for investigating mechanisms underlying multiple sclerosis and for evaluating immunomodulatory therapeutics.
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The multi-antigen induction system has been refined. It supports the use of classic myelin antigens such as MOG, CFA, and PTX, combined with Freund’s adjuvant for induction, making it suitable for diverse research applications. |
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Immune induction is stable and controllable. Standardized immunization protocols control the antigen dose and adjuvant ratio, thereby enhancing the consistency of disease onset and the success rate. |
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The neurological function scoring system is well-established. It can reliably assess typical neurological phenotypes, including caudal weakness, hindlimb paralysis, and motor coordination deficits. |
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Pathological features closely resemble clinical findings. It can reliably reproduce the core pathological features, including inflammatory cell infiltration, demyelination, and axonal damage in the central nervous system. |
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The model exhibits high reproducibility. Standardize immunization and husbandry management protocols to minimize batch-to-batch variability and enhance data reliability. |
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The multidimensional evaluation system has been refined. Systematic evaluation is achieved by integrating behavioral scoring, histopathological findings, and immunological parameters. |
| Modeling cycle | 6–8 weeks |
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C57BL/6 female mice |
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Classic positive‑acting drugs include glucocorticoids, immunomodulators, S1P receptor modulators, and anti‑cell migration antibodies. |
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It is primarily used for drug development and efficacy evaluation in multiple sclerosis (MS), while also being extensively applied to basic and translational research on central nervous system autoimmune mechanisms, demyelination and remyelination processes, blood–brain barrier function, and neuroimmune interactions. It represents the most important experimental model system for studying CNS autoimmune diseases. |
Experimental results
Construction of an EAE animal model
01 Prepare the antigen and mix it with an adjuvant to form an antigen emulsion.
02 Rats were injected with an antigen emulsion at the plantar surface (footpad), while mice received a subcutaneous injection of the antigen emulsion on the dorsal side of the spine. A second injection of pertussis toxin was administered 48 hours later.
03 The day of injection is designated as Day 0. Body weight and clinical neurological function scores (using the Knono scoring system) are recorded daily until 30 days post‑immunization.
EAE symptom score
Mouse body weight changes
Unlike the control group mice, which exhibited a steady and sustained increase in body weight, EAE model mice experienced a rapid initial decline in body weight, followed by a modest short-term rebound before returning to a sustained downward trend. By day 30 post‑induction, a significant statistical difference in body weight change was observed between the two groups, indicating that EAE induction resulted in marked weight loss in the mice and confirming the validity of the model.
Results of HE staining and LFB myelin staining
Compared with the spinal cord tissue of mice in the control group, the spinal cords of EAE model mice exhibited extensive inflammatory cell infiltration on hematoxylin–eosin staining, with pronounced tissue‑related inflammatory damage. LFB myelin staining revealed a marked lightening and reduction in the area of blue‑stained myelin, indicative of significant demyelination, accompanied by neuronal loss and injury, thereby confirming that the EAE model successfully induces central nervous system inflammation, demyelination, and neuronal damage.

















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