Multiple Sclerosis

The SCH-induced Experimental Autoimmune Encephalomyelitis (EAE) model is a robust and well-established model of Multiple Sclerosis, induced in DA rats using spinal cord homogenate from naïve animals emulsified in Incomplete Freund’s Adjuvant (IFA).

This model leads to a severe, relapsing, and demyelinating form of encephalomyelitis. Clinical signs develop in an ascending manner—initially presenting as tail flaccidity (score 1–2), followed by progressive hind limb paralysis (score 3–6), forelimb involvement (score 7), and in severe cases, quadriplegia and death (score 8).

Disease pathology is mediated by CD4⁺ T cells and involves both Th1 and Th17 immune responses. Histological analysis at termination reveals significant demyelination of the central nervous system, making this model highly relevant for evaluating neuroinflammation and CNS-targeted therapies.

Key Features:

• Severe, relapsing disease course with reproducible clinical scoring
• CD4⁺ T cell-dependent; driven by both Th1 and Th17 cells
• CNS demyelination confirmed by histology
• Suitable for assessment of IL-17 and IFN-γ responses ex vivo
• Allows foradoptive transfer of autoreactive CD4⁺ T cells following ex vivo re-stimulation

The SCH-EAE model is a powerful tool for mechanistic studies and evaluation of immunomodulatory therapies targeting T cell function or demyelinating pathology. For study outlines, readouts, and technical specifications, please contact us or refer to our detailed model information sheets.

MOG1–125-induced Experimental Autoimmune Encephalomyelitis (EAE) is induced in DA rats using recombinant myelin oligodendrocyte glycoprotein (MOG1–125) emulsified in Incomplete Freund’s Adjuvant (IFA). This antigen-specific model offers a more targeted immune response than spinal cord homogenate and is widely used to study both T and B cell contributions to central nervous system (CNS) autoimmunity.

The disease course is typically chronic and may present as either monophasic or relapsing, depending on the immunization protocol and animal strain. Clinical symptoms begin with tail weakness, progressing to hind limb paralysis, with disease severity scored on a standardized scale.

MOG1–125-induced EAE is CD4⁺ T cell-mediated and characterized by strong Th1 and Th17 responses. The model also induces a humoral response against MOG, making it particularly valuable for evaluating therapies targeting both cellular and antibody-mediated mechanisms.

Key Features:

• Antigen-specific model with defined immune target (MOG1–125)
• Chronic disease course with potential relapses
• Involves both T cell- and B cell-mediated immune responses
• CD4⁺ T cell dependency allows for adoptive transfer experiments
• Suitable for ex vivo assessment of IL-17 and IFN-γ responses
• Histological analysis reveals demyelination and inflammatory infiltration in CNS

This model is ideal for therapeutic evaluation in both acute and chronic stages of MS-like disease, particularly for agents targeting myelin-specific immune responses.

Myelin Basic Protein (MBP)-induced Experimental Autoimmune Encephalomyelitis (EAE) is established in Lewis or DA rats through immunization with MBP emulsified in Incomplete Freund’s Adjuvant (IFA). This is one of the earliest and most well-characterized EAE models, offering high reproducibility and a well-defined immune response.

The disease onset is typically rapid, with animals developing acute ascending paralysis that may resolve spontaneously or transition into a relapsing course depending on strain and protocol. Clinical scoring reflects progression from tail flaccidity to full hind limb and, in some cases, forelimb involvement.

The model is mediated by autoreactive CD4⁺ T cells and strongly driven by Th1 responses, with some Th17 contribution. CNS pathology includes inflammation and demyelination, primarily in the spinal cord.

Key Features:

• Acute or relapsing disease course depending on strain and immunization
• Highly reproducible and antigen-specific
• Strong CD4⁺ T cell-mediated inflammation
• Robust Th1 response; suitable for testing anti-inflammatory and T cell-targeting therapies
• CNS demyelination detectable by histology
• Compatible with adoptive transfer studies using MBP-reactive CD4⁺ T cells

MBP-induced EAE provides a reliable and immunologically well-defined platform for investigating early immune mechanisms in CNS autoimmunity and evaluating immunomodulatory treatments.

The MOG35–55-induced Experimental Autoimmune Encephalomyelitis (EAE) model is one of the most widely used mouse models for studying Multiple Sclerosis. It is typically established in C57BL/6 mice by immunization with the MOG35–55 peptide emulsified in Complete Freund’s Adjuvant (CFA), followed by pertussis toxin administration.

This antigen-specific, CD4⁺ T cell-mediated model induces a chronic, monophasic disease characterized by ascending paralysis, beginning with tail weakness and progressing to hind limb and, in some cases, forelimb involvement. Onset typically occurs 9–12 days post-immunization.

MOG35–55 EAE is driven primarily by Th1 and Th17 responses, with significant inflammatory infiltration and demyelination in the spinal cord and brain. The model is highly reproducible and well suited for evaluating therapeutics targeting T cells, cytokine pathways, and demyelination.

Key Features:

• Chronic, monophasic disease with reproducible onset and progression
• Antigen-specific model using defined MOG35–55 peptide
• Strong CD4⁺ T cell and Th17-driven pathology
• CNS demyelination and inflammation confirmed by histology
• Suitable for ex vivo readouts of cytokine production (e.g., IL-17, IFN-γ)
• Widely used for mechanistic studies and preclinical drug testing in MS

This model is ideal for evaluating therapeutic candidates that modulate adaptive immunity, particularly CD4⁺ T cell responses, and for assessing long-term efficacy in chronic neuroinflammation.

The PLP-induced Experimental Autoimmune Encephalomyelitis (EAE) model is a well-established relapsing-remitting MS model induced in SJL/J mice. Disease is triggered by immunization with the PLP139–151 peptide emulsified in Complete Freund’s Adjuvant (CFA), typically followed by pertussis toxin administration.

This model closely mimics the relapsing-remitting clinical course seen in many MS patients. After an acute onset of ascending paralysis, animals often enter remission followed by one or more spontaneous relapses. The relapsing disease course makes this model particularly suitable for studying long-term efficacy, immune memory, and reactivation mechanisms.

PLP-induced EAE is mediated by CD4⁺ T cells and involves both Th1 and Th17 responses. CNS pathology includes inflammation, demyelination, and immune cell infiltration, particularly in the spinal cord and brainstem.

Key Features:

• Relapsing-remitting disease course mimicking human MS
• Induced in SJL/J mice with PLP139–151 peptide
• Strong CD4⁺ T cell-mediated inflammation
• Involves both Th1 and Th17 responses
• Suitable for studying disease reactivation and immune memory
• CNS demyelination and pathology can be assessed by histology

This model is ideal for evaluating therapies aimed at preventing relapse, promoting long-term remission, or modulating T cell responses in chronic MS-like disease.