Effects of glatiramer acetate on chemokine expression in ms models immunized with different myelin antigens

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system with autoimmune aetiology. Experimental autoimmune encephalomyelitis (EAE) is a model of MS that can be induced in several species by different myelin-related auto-antigens, such as myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), and myelin proteolipid protein (PLP).Glatiramer acetate (GA) (Copaxone®) is a disease-modifying drug approved for the treatment of relapsing-remitting MS. The mechanism of action of GA in MS and EAE is not fully elucidated.The objective of this study is to determine whether GA will also act on chemokine expression in EAE which induced by MOG35-55, MBP68-82, and PLP139-151. Female mices were devided six groups and immunized with MOG, MBP, and PLP peptides. Normal and unimmunized animals were used as control. In GA-treatment groups (three group immunized with different antigenic peptide), GA was injected on day 7th before immunization with MBP, PLP and MOG. Animals were killed by cervical dislocation at days 14. RANTES/CCL5, MIP2/CXCL2-3 ve IP-10/CXCL10 chemokines were measured using the appropriate ELISA kits in treated and non-treated groupsWe observed significantly increased expression of chemokines all non-treatment groups immunized with different antigen according to normal controls. In GA-treated groups, chemokine expression is almost to the baseline level observed in control animals.Our data suggest that in vivo therapy with glatiramer acetate causes a statistically significant reduction in the expression of chemokines associated with Th1 cell homing.