More MS news articles for Mar 2002

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

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11880161&dopt=Abstract

J Neuroimmunol 2002 Feb;123(1-2):170-9
Iarlori C, Reale M, De Luca G, Di Iorio A, Feliciani C, Tulli A, Conti P, Gambi D, Lugaresi A.
Department of Oncology and Neuroscience, Neuroimmunology Unit, University "G. d'Annunzio", Via dei Vestini, I-66013, Chieti, Italy

Monocyte chemoattractant protein-1 (MCP-1) seems to be involved in the pathogenesis of multiple sclerosis (MS).

We found that in unstimulated (PHA(minus sign)) and PHA-stimulated (PHA(+)) peripheral blood mononuclear cells (PBMC), MCP-1 and TNFalpha levels are higher in stable untreated MS patients.

Interferon gamma (IFNgamma) is higher in relapsing patients in PHA(minus sign) cultures and in stable patients in PHA(+) cultures.

Chronic IFNbeta-1b treatment down-regulates TNFalpha, IFNgamma and MCP-1 production except for TNFalpha in relapsing patients.

IFNbeta-1b, in vitro, increases MCP-1, TNFalpha and IFNgamma spontaneous production in all patients.

Multivariate analysis suggests that MCP-1 production is dependent from clinical status and not from TNFalpha and IFNgamma 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.