Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant

• Published in: Clinical and experimental immunology 2004-04, Vol.136 (1), p.49-55
• Main Authors: STOSIC‐GRUJICIC, S., RAMIC, Z., BUMBASIREVIC, V., HARHAJI, L., MOSTARICA‐STOJKOVIC, M.
• Format: Article
• Language: English
• Subjects: adjuvants; Animal Studies; Animals; Biological and medical sciences; complete Freund's adjuvant; Dark Agouti rats; Disease Models, Animal; Disease Susceptibility; Encephalomyelitis, Autoimmune, Experimental - etiology; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - pathology; experimental autoimmune encephalomyelitis; Female; Freund's Adjuvant; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Immunopathology; Lymphocyte Activation - immunology; Male; Medical sciences; Multiple Sclerosis - immunology; Rats; Rats, Inbred Strains; Spinal Cord - immunology; Spinal Cord - pathology; T lymphocytes; T-Lymphocytes - immunology; Tissue Extracts - immunology
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.2004.02418.x

SUMMARY Experimental autoimmune encephalomyelitis (EAE) is a well‐recognized model for multiple sclerosis (MS) in humans. However, adjuvants used with encephalitogens to induce EAE produce non‐specific effects interfering with the mechanisms involved in the autoimmune response to the central nervous system (CNS) tissue. It is therefore important to establish a more suitable model of EAE for analysis of autoimmune phenomena resembling those operative in MS. Here we report that EAE can be induced regularly in Dark Agouti (DA) strain of rats with spinal cord tissue without any adjuvant, as judged by both clinical and histological parameters. The incidence and severity of EAE depended on the origin of the encephalitogen, the rat versus guinea pig spinal cord homogenate being more efficient. Furthermore, EAE could be reinduced in animals which had recovered from disease that had been induced actively with encephalitogen alone, suggesting the role of adjuvant‐generated non‐specific mechanisms in resistance to reinduction of EAE. Thus, EAE induced in DA rats with encephalitogen alone provides a reproducible model for defining pathogenically relevant events in CNS autoimmunity devoid of the potentially misleading effects of adjuvants.