Journal of Neuroimmunology, 36 (1992) 105-115 105 © 1992 Elsevier Science Publishers B.V. All rights reserved 0165-5728/92/$05.00 JNI 02108 Effect of anti-interferon-7 and anti-interleukin-2 monoclonal antibody treatment on the development of actively and passively induced experimental allergic encephalomyelitis in the SJL/J mouse Trang T. Duong a,,, Joanne St. Louis ", Joseph J. Gilbert b, Fred D. Finkelman c and Gill H. Strejan a Department of Microbiology and Immunology, the Robarts Research Institute, Unit,ersity of Western Ontario, London, Ontario NOA 5C1, Canada, h Department of Pathology, Victoria Hospital, London, Ontario, Canada, and c Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA (Received 17 July 1991) (Revised, received 14 August 1991) (Accepted 26 August 1991) Key words: Experimental allergic encephalomyelitis; Lymphokines(interferon-y, interleukin-2); Anti-lymphokine monoclonal anti- bodies; (SJL/J mouse) Summary SJL/J mice challenged with myelin basic protein (MBP) in complete Freund's adjuvant (CFA) developed only mild chronic-relapsing experimental allergic encephalomyelitis (EAE) with very low incidence. However, treatment of challenged mice with anti-interferon-7 (IFN- 7) monoclonal antibody (mAb) determined severe disease in all cases. Similarly, in passive EAE, the addition of anti-IFN-7 to the in vitro MBP-activated cells at the time of transfer led to significant disease exacerbation in all recipients. The disease enhancing effect was observed only when the mAb was given at the time of active challenge or of passive transfer, but not at later times. Anti-interleukin-2 (IL-2) antibody had only a marginal effect in the active induction, but drastically reduced the manifestations of passive EAE, even when mixed with a disease-enhancing dose of anti-IFN-y. These findings support the notion that IL-2 is required for disease induction whereas IFN-7 plays a disease-limiting role early in the development of EAE. Correspondence to: Dr. G.H. Strejan, Department of Mi- crobiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada. * Supported by a Multiple Sclerosis Society of Canada Re- search studentship. This study was supported by the MS Society of Canada. Introduction Experimental allergic encephalomyelitis (EAE) is an autoimmune inflammatory and demyelinat- ing disease of the central nervous system (CNS), and is considered the best available animal coun-