Abstract
RANTES (regulated upon activation, normal T-cell expressed and secreted), a CC chemokine, appears to play a role in the pathogenesis of relapsing-remitting multiple sclerosis (RR-MS), enhancing the inflammatory response within the nervous system. We have demonstrated that RANTES production is increased in RR-MS compared to controls. Interferon-beta-1b (IFN-beta-1b) treatment reduces RANTES production in sera and peripheral blood adherent mononuclear cell (PBAM) supernatants both in relapse and remission. IFN-beta-1b also reduces RANTES expression in PBAM. Our results suggest that RANTES modulation might represent one of the mechanisms of action of IFN-beta-1b in RR-MS.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adjuvants, Immunologic / therapeutic use*
-
Adult
-
Chemokine CCL5 / biosynthesis
-
Chemokine CCL5 / blood
-
Chemokine CCL5 / genetics
-
Chemokine CCL5 / metabolism*
-
Female
-
Humans
-
Interferon beta-1a
-
Interferon beta-1b
-
Interferon-beta / therapeutic use*
-
Male
-
Middle Aged
-
Monocytes / drug effects
-
Monocytes / metabolism
-
Multiple Sclerosis, Relapsing-Remitting / blood
-
Multiple Sclerosis, Relapsing-Remitting / drug therapy*
-
Multiple Sclerosis, Relapsing-Remitting / metabolism*
-
Phytohemagglutinins / pharmacology
-
RNA, Messenger / metabolism
-
Reverse Transcriptase Polymerase Chain Reaction
Substances
-
Adjuvants, Immunologic
-
Chemokine CCL5
-
Phytohemagglutinins
-
RNA, Messenger
-
Interferon beta-1b
-
Interferon-beta
-
Interferon beta-1a