Experimental autoimmune encephalomyelitis kit
SB-PEPTIDE offers a turnkey solution for multiple sclerosis (MS) studies with an experimental autoimmune encephalomyelitis kit (EAE kit). Each kit provided allows the induction of EAE in 9 mice (0.2mL/mouse). The kit contains 2.1mL of a ready-to-use MOG35-55/CFA emulsion, one vial containing 5µg pertussis toxin (PTX) in glycerol buffer and a recommended experimental protocol with typical results.
Myelin Oligodendrocyte Glucoprotein (MOG35-55) is used in emulsion with Complete Freund’s Adjuvant (CFA) in EAE studies. Emulsification is an important step in the success of the EAE induction, results will partially depend on this phase. SB-PEPTIDE offers a ready-to-use MOG35-55/CFA emulsion.
The complete Freund’s adjuvant is used as an immunopotentiator, it is composed of inactivated and dried mycobacteria and used with MOG 35-55 to induce EAE. Experimental autoimmune encephalomyelitis is the model commonly used to study efficacy of drugs for treatment of multiple sclerosis (MS) but also pathogenesis of autoimmunity, CNS inflammation, demyelination, cell trafficking and tolerance induction.
EAE induction kit specifications
|MOG35-55 concentration : 1 mg/mL
Mycobacterium tuberculosis concentration: 1 mg/mL
|Each kit provides enough to induce EAE in 9 mice|
The kit contains 3 tubes with 0.7mL of pre-filled MOG/CFA emulsion, one vial containing 5µg pertussis toxin (PTX) in glycerol buffer and a recommended experimental protocol
Recommended syringe and needles (not included): 1mL syringe with needle 19Gx1 1/2″ – 1,1 x 40 mm for emulsion suction and 22G x 1 1/4″, 0.7 x 30 mm needle for administrations
|MOG35-55 : MEVGWYRSPFSRVVHLYRNGK – Synthesized by SB-PEPTIDE – see MOG35-55 peptide product page|
|Product catalog||Size||Price € HT||Price $ USD|
Customized EAE induction kit
SB-PEPTIDE offers to prepare customized EAE induction kit, with various antigen peptides (see SB-PEPTIDE’s EAE peptide range here) with specific concentrations of antigen and CFA. Contact us for more details.
References & citations
J Neurosci Methods. 2022 Feb 1;367:109443. doi: 10.1016/j.jneumeth.2021.109443. Epub 2021 Dec 15
Application note: Effect of CFA contration on EAE induction
Experimental autoimmune encephalomyelitis (EAE) is one of the most popular animal models of multiple sclerosis (MS). Mouse models of demyelinating diseases have been useful in both the demonstration of T cellmediated demyelination and in the characterization of the pathogenesis of immune-mediated demyelinating disease. EAE is a CD4 + T cell-mediated, demyelinating autoimmune disease of the CNS that is characterized by mononuclear cell infiltration. EAE can be induced by various antigens including MOG35-55, a peptide derived from the Myelin Oligodendrocyte Glycoprotein, a structural protein in the myelin sheath. The injection of this peptide emulsified with CFA in mice induces a production of anti-MOG antibodies that cause demyelination and a chronic EAE. The purpose of this study was to investigate the influence of CFA amount on EAE induction.
1-Androutsou, M.-E., Tapeinou, A., Vlamis-Gardikas, A. & Tselios, T. Med. Chem. 14, 120–128 (2018)
BACKGROUND: Myelin oligodendrocyte glycoprotein (MOG) is located on the external surface of myelin, a membranous component of the central nervous system (CNS) that forms the insulating lipid layer around neurons. The major MOG splicing variant (a1 transcript) encodes a transmembrane protein with an extracellular domain of an Ig variable (IgV) fold. MOG IgV domains from the same or different cells dimerize and contribute to the organization and maintenance of the myelin sheath in neurons. The encepalitogenic T cells recognize MOG and its immunodominant epitopes (epitopes 1-22, 35-55 and 92-106 located at the dimer interface) as foreign antigens and cause the destruction of myelin (demyelination) leading to the clinical condition known as multiple sclerosis (MS). Recognition of the antigen takes place in the context of the trimolecular complex formed by HLA, MOGpeptides and TCR.
OBJECTIVE: Understanding the role of MOG in MS.
METHOD/RESULTS: We have reviewed herein, the genomic organization of the human MOG gene, the structural characteristics of the MOG protein, the involvement of MOG in MS and clinical studies for the treatment of MS based on MOG peptide analogues.
CONCLUSION: Conjugates of antigenic MOG peptides to mannan and combinations of antigenic MOG and other peptides chemically linked to cells of the immune system may modify the immune response, alleviating in some cases the symptoms of MS.