Interferon β1b modulates MCP-1 expression and production in relapsing-remitting multiple sclerosis

Abstract
Monocyte chemoattractant protein-1 (MCP-1) seems to be involved in the pathogenesis of multiple sclerosis (MS). We found that in unstimulated (PHA−) and PHA-stimulated (PHA+) peripheral blood mononuclear cells (PBMC), MCP-1 and TNFα levels are higher in stable untreated MS patients. Interferon gamma (IFNγ) is higher in relapsing patients in PHA− cultures and in stable patients in PHA+ cultures. Chronic IFNβ-1b treatment down-regulates TNFα, IFNγ and MCP-1 production except for TNFα in relapsing patients. IFNβ-1b, in vitro, increases MCP-1, TNFα and IFNγ spontaneous production in all patients. Multivariate analysis suggests that MCP-1 production is dependent from clinical status and not from TNFα and IFNγ production. Logistic regression analysis shows that MCP-1 production is significantly modified by treatment. Further studies are needed to clarify the role of MCP-1 in MS.

Keywords
Multiple sclerosis; MCP-1; TNFα; IFNγ; IFNβ; Peripheral blood mononuclear cells