| First Author | Jiang Z | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 3 | Pages | 789-99 |
| PubMed ID | 19224632 | Mgi Jnum | J:146789 |
| Mgi Id | MGI:3838447 | Doi | 10.1002/eji.200838427 |
| Citation | Jiang Z, et al. (2009) MOG(35-55) i.v suppresses experimental autoimmune encephalomyelitis partially through modulation of Th17 and JAK/STAT pathways. Eur J Immunol 39(3):789-99 |
| abstractText | Intravenous (i.v.) administration of encephalitogenic peptide can effectively prevent experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis; however, the underlying cellular and molecular mechanisms are not fully understood. In this study, we induced i.v. tolerance to EAE by administration of MOG(35-55) peptide and determined the effect of this approach on intracellular signaling pathways of the IL-23/IL-17 system, which is essential for the pathogenesis of MS/EAE. In tolerized mice, phosphorylation of JAK/STAT-1, -4, ERK1/2 and NF-kappaBp65 were significantly reduced in splenocytes and the central nervous system. MOG i.v. treatment led to significantly lower production of IL-17, and administration of exogenous IL-17 slightly broke immune tolerance, which was associated with reduced activation of STAT4 and NF-kappaB. Suppressed phosphorylation of these pathway molecules was primarily evident in CD11b(+) and small numbers of CD4(+), CD8(+) and CD11c(+) cells. More importantly, adoptive transfer of CD11b(+) splenocytes of tolerized mice effectively delayed onset and reduced clinical severity of actively induced EAE. This study correlates MOG i.v. tolerance with modulation of Jak/STAT signaling pathways and investigates novel therapeutic avenues for the treatment of EAE/MS. |
