IFN-beta suppresses experimental autoimmune neuritis in Lewis rats by inhibiting the migration of inflammatory cells into peripheral nervous tissue

The putative prophylactic and therapeutic effect of interferon-beta (IFN-be ta) on autoimmune inflammation of the peripheral nervous system was evaluat ed in experimental autoimmune neuritis (EAN), a well-known animal model of the human Guillain-Barre syndrome (GBS), We report that treatment of rats w ith 300,000 U of recombinant rat IFN-beta (rrIFN-beta) given every other da y starting at the day of immunization prevented clinical signs of EAN, When treatment was started at the onset of disease development, the cytokine cl early ameliorated EAN, Both B- and T-cell responses towards peripheral myel in were suppressed by the IFN-beta, and immunohistochemical analyses reveal ed a strong decrease in the numbers of infiltrating CD4(+) T cells, macroph ages, and other inflammatory cells as well as a significant reduction in MH C class II antigen expression and monocyte chemotactic protein-1 (MCP-1) pr oduction, which induces chemotaxis and chemokinesis of leukocytes from bloo d. It is concluded that the observed suppression of EAN by rrIFN-beta is as sociated with a decrease in the migration of inflammatory cells into periph eral nervous tissue. J, Neurosci, Res. 56:123-130, 1999, (C) 1999 Wiley-Lis s, Inc.