Inflammatory
cytokines are implemented in the pathogenesis of
experimental autoimmune encephalomyelitis (EAE), an animal model of
multiple sclerosis. We previously demonstrated that
glia maturation factor (
GMF), a brain
protein, isolated, sequenced and cloned in our laboratory, induce expression of proinflammatory
cytokine/
chemokine in the central nervous system (CNS). We found
GMF-deficient (knockout) mice relatively resistant to EAE development after immunization with encephalitogenic MOG
peptide 35-55. Consistent with these findings, the expression of proinflammatory
cytokines in CNS of mice with EAE differed profoundly between wild type and
GMF-knockout mice. In the present study we examined the expressions of six murine signal transducers and activators of transcription (STATs) genes, which are known to regulate the
cytokine-dependent signal transduction pathways in autoimmune
inflammation. The expressions of STATs genes were evaluated in the brains and spinal cords of wild type and
GMF-knockout mice at the peak of EAE by quantitative real-time RT-PCR. Compared to
GMF-knockout mice, the expressions of STAT1, STAT2, STAT3, STAT4, STAT5, and STAT6 genes were significantly (P < 0.001) upregulated in the wild type mice exhibiting EAE symptoms. The results are consistent with the diminished development of EAE in the
GMF-knockout mice. A significant suppression of STATs expression in
GMF-knockout mice suggests
GMF as an upstream effector of JAK/STAT signaling.