THE DEVELOPMENT OF AUTOIMMUNE ENCEPHALOMYELITIS PROVOKED BY MYELIN OLIGODENDROCYTE GLYCOPROTEIN IS ASSOCIATED WITH AN UP-REGULATION OF BOTHPROINFLAMMATORY AND IMMUNOREGULATORY CYTOKINES IN THE CENTRAL-NERVOUS-SYSTEM
Y. Okuda et al., THE DEVELOPMENT OF AUTOIMMUNE ENCEPHALOMYELITIS PROVOKED BY MYELIN OLIGODENDROCYTE GLYCOPROTEIN IS ASSOCIATED WITH AN UP-REGULATION OF BOTHPROINFLAMMATORY AND IMMUNOREGULATORY CYTOKINES IN THE CENTRAL-NERVOUS-SYSTEM, Journal of interferon & cytokine research, 18(6), 1998, pp. 415-421
Experimental autoimmune encephalomyelitis (EAE) is an inflammatory dis
ease of the central nervous system (CNS), We previously reported upreg
ulation of gene expression for a number of proinflammatory cytokines,
interleukin-1 beta (IL-1 beta), IL-2, IL-6, tumor necrosis factor-alph
a (TNF-alpha), TNF-beta, and interferon-gamma (IFN-gamma), in the CNS
of mice with myelin basic protein (MBP)-induced relapsing EAE by using
semiquantitative reverse transcriptase-polymerase chain reaction (RT-
PCR), However, in these mice there was no significant increase of gene
expression for immunoregulatory cytokines (IL-4, IL-10, transforming
growth factor-beta [TGF-beta]), We report here that gene expression fo
r both proinflammatory and immunoregulatory cytokines increased during
the course of disease in the CNS of mice with myelin oligodendrocyte
glycoprotein (MOG)-induced non-relapsing EAE, These results indicate t
hat the gene expression pattern of immunoregulatory cytokines in the C
NS may be different between MBP-induced and MOG-induced EAE and that i
t may influence the type of disease. Accordingly, the course of the di
sease may be influenced by the interplay between the proinflammatory a
nd immunoregulatory cytokines.