Non-coding plasmid DNA induces γ-IFN in vivo and suppresses autoimmune encephalomyelitis

G. L. Boccaccio, E. Stibbe, F. Mor, L. Steinman

Research output: Contribution to journalArticlepeer-review


Experimental autoimmune encephalomyelitis (EAE) serves as a model for human multiple sclerosis, a demyelinating disease mediated by CD4+ T cells targeted to various myelin components. Attempts to control the disease by using DNA vaccines are under study. We report treatment with plasmid DNA carrying no insert abrogated the disease induced in Lewis rats by the myelin basic protein (MBP) peptide 87-99. No clinical manifestation of disease nor infiltration were observed after injection of plasmid vectors, whereas calf thymus DNA did not influence the incidence or severity of EAE. The encephalitogenic capacity of splenocytes was largely reduced. Significant differences were observed when the expression of both anti- and pro-inflammatory cytokines was analyzed. Both TGF-β and IL-10 mRNAs appeared five-fold elevated in the pECE-treated animals, while the expression of TNF-α was slightly reduced. The levels of γ-IFN were augmented in anti-MBP lymphnode cells from protected animals. This cytokine has both a pro-inflammatory and a regulatory role in EAE. It has been reported that certain inmunostimulatory DNA sequences containing CpG motifs can stimulate the secretion of this and other cytokines. Several copies of those motifs are present in the plasmids showing protective effects. Therefore, it is likely that the injection of naked plasmid DNA suppresses EAE by inducing γ-IFN.

Original languageEnglish
Pages (from-to)A1102
JournalFASEB Journal
Issue number5
StatePublished - 20 Mar 1998


Dive into the research topics of 'Non-coding plasmid DNA induces γ-IFN in vivo and suppresses autoimmune encephalomyelitis'. Together they form a unique fingerprint.

Cite this