Glia maturation factor (
GMF), a
protein primarily localized in the central nervous system (CNS) was isolated, sequenced and cloned in our laboratory. We previously demonstrated that
GMF mediates the
experimental autoimmune encephalomyelitis (EAE)-induced production of pro-inflammatory
cytokines and
chemokines in the central nervous system of mice. In the present study we show that immunization with
myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55) caused an early onset (days 7-9 post immunization) and severe EAE with a mean peak score of 3.5 ± 0.5 in mice. Neutralization of
GMF with four
injections of anti-
GMF antibody 5 to 11 days post immunization delayed the time of onset (days 12-14 post immunization) and significantly reduced the severity of EAE (mean peak score of 1.5 ± 0.4). Consistent with these clinical scores, histological examination of the CNS of these mice revealed profound differences between
GMF-antibody treated mice and isotype matched control-antibody treated mice. Histological analysis of the spinal cord and brain showed severe
inflammation and
demyelination in the control antibody-treated mice whereas significantly reduced
inflammation and
demyelination was detected in
GMF-antibody-treated mice at days 8, 16, and 24 post immunization. The decreased incidence and reduced severity of EAE in
GMF-antibody-treated mice was consistent with the significantly reduced expressions of pro-inflammatory
cytokines and
chemokines. Our overall results demonstrate that neutralization of endogenous
GMF with an affinity purified
GMF antibody significantly decreased the
inflammation, severity and progression of immunization induced active, passive and relapsing-remitting EAE. Treatment of mice with isotype-matched control antibody did not have any effect on EAE. Taken together, these results demonstrate the critical role of
GMF in EAE, and
GMF antibody as a potent anti-inflammatory therapeutic agent for effectively suppressing EAE in mouse models of major types of
multiple sclerosis (MS).