Protracted, relapsing and demyelinating experimental autoimmune encephalomyelitis in DA rats immunized with syngeneic spinal cord and incomplete Freund's adjuvant

• Published in: Journal of neuroimmunology Vol. 63; no. 2; pp. 193 - 205
• Main Authors: Lorentzen, Johnny C., Issazadeh, Shohreh, Storch, M., Mustafa, Maha I., Lassman, Hans, Linington, Christopher, Klareskog, Lars, Olsson, Tomas
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 31-12-1995
• Subjects: Amino Acid Sequence; Animals; Autoantibodies - biosynthesis; Central nervous system; Demyelinating Diseases - immunology; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental - immunology; Freund's Adjuvant - pharmacology; Guinea Pigs; Immunization; Immunohistochemistry; Injections, Subcutaneous; Medicin och hälsovetenskap; Molecular Sequence Data; Multiple sclerosis; Myelin basic protein; Myelin Basic Protein - pharmacology; Myelin Proteins; Myelin-Associated Glycoprotein - pharmacology; Myelin-Oligodendrocyte Glycoprotein; Peptides - pharmacology; Phenotype; Rats; Rats, Inbred Strains; Recurrence; Reproducibility of Results; Spinal Cord - immunology; Spinal Cord - pathology; T cells; Time Factors; Multiple sclerosis; T cells; Myelin basic protein; Central nervous system
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/0165-5728(95)00153-0

Experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis (MS). However, MS is a chronic, relapsing and demyelinating disease, whereas EAE in rats is typically a brief and monophasic disorder showing little demyelination. We demonstrate here that DA rats develop severe, protracted and relapsing EAE (SPR-EAE) after a subcutaneous immunization at the tail base with syngeneic spinal cord and incomplete Freund's adjuvant (IFA). The neurological deficits were accompanied by demyelinating inflammatory lesions in the spinal cord, with infiltrating T lymphocytes and perivascular deposition of immunoglobulins and complement. The induction of SPR-EAE was associated with humoral autoreactivity to myelin oligodendrocyte glycoprotein (MOG) and cellular autoreactivity to the rat myelin basic protein (MBP) peptides 69–87 and 87–101. These two peptides, as well as whole rat MBP, were encephalitogenic. In conclusion, we believe that the presently described demyelinating SPR-EAE represents a useful model for MS.