Costimulatory Molecule Expression on Leukocytes from Mice with Experimental Autoimmune Encephalomyelitis Treated with IFN- β

• Published in: Journal of interferon & cytokine research Vol. 23; no. 6; pp. 293 - 298
• Main Authors: Hallal, Dannie E.M., Farias, Alessandro S., Oliveira, Elaine C., Diaz-Bardales, Blanca Maria, Brandão, Carlos Otavio, Protti, Gustavo G., Pereira, Fernanda G., Metze, Irene L., Santos, Leonilda M.B.
• Format: Journal Article
• Language: English
• Published: United States Mary Ann Liebert, Inc 01.06.2003
• Subjects: Animals; Antigens, CD; Antigens, Differentiation - metabolism; B7-1 Antigen - metabolism; CTLA-4 Antigen; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - therapy; Female; Interferon-beta - pharmacology; Interferon-beta - therapeutic use; Lymphocyte Activation - drug effects; Mice; Multiple Sclerosis - immunology; Multiple Sclerosis - therapy; T-Lymphocytes - drug effects; T-Lymphocytes - immunology
• ISSN: 1079-9907; 1557-7465
• DOI: 10.1089/107999003766628133

Interferon-beta (IFN-beta) is of benefit in the treatment of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), but the mechanisms by which it exerts this beneficial effect remain uncertain. The present data demonstrate that IFN-beta therapy impairs the proliferative response to concanavalin A (ConA) and myelin basic protein (MBP), decreases expression of the CD80 molecule on leukocytes of treated mice, and may thereby impede the Th1 cell activation-promoting anergy in EAE. Moreover, IFN-beta therapy increases expression of the CTLA4 molecule, which induces a counterregulatory Th2 response. The reduction of CD80 expression with concomitant increase of CTLA4 expression alters the course of EAE and may be useful as a monitor in therapy with IFN-beta.