Yet another action of glaterimer acetate. It is affect the function of natural killer cells,is this important to the action of glaterimer acetate. These guys natural function is to fight infection and get rid of tumors... Dacluzimab affects NK function but is much more active at limiting relapse rate. What doesn't it do? Not much by the look of it so in another study
Sellner J, Koczi W, Harrer A, Oppermann K,
Obregon-Castrillo E, Pilz G, Wipfler P, Afazel S, Haschke-Becher E,
Trinka E, Kraus J.
Glatiramer acetate attenuates the pro-migratory profile of adhesion molecules on various immune cell subsets in multiple sclerosis.
Clin Exp Immunol. 2013 Apr. doi: 10.1111/cei.12125. [Epub ahead of print]
An altered expression pattern of adhesion molecules (AM) on the surface of immune cells is a premise for their extravasation into the central nervous system (CNS) and the formation of acute brain lesions in multiple sclerosis (MS). We evaluated the impact of glatiramer acetate (GA) on cell-bound and soluble AM in the peripheral blood of patients with relapsing-remitting MS (RRMS). Fifteen patients treated de-novo with GA were studied on four occasions over a period of 12 months. Surface levels of ICAM-1, ICAM-3, LFA-1 and VLA-4 were assessed in T cells (CD3+CD8+, CD3+CD4+), B cells, natural killer (NK) cells, natural killer T cells (NKT) and monocytes by 5-colour flow cytometry. Soluble E-selectin, ICAM-1, ICAM-3, PECAM-1, P-selectin and VCAM-1 were determined with a fluorescent bead-based immunoassay. The pro-migratory pattern in RRMS was verified by comparison with healthy controls and was characterized by an up-regulation of LFA-1 (CD3+CD4+ T cells, B cells), VLA-4 (CD3+CD8+ T cells, NK cells), ICAM-1 (B cells) and ICAM-3 (NK cells). Effects of GA treatment were most pronounced after 6 months and included attenuated levels of LFA-1 (CD3+CD4+) and VLA-4 (CD3+CD4+, CD3+CD8+, NK, NKT, monocytes). Further effects included a lowering of ICAM-1 and ICAM-3 levels in almost all immune cell subsets. Soluble AM levels in RRMS did not differ from healthy controls and remained unaltered after GA treatment. The de-regulated pro-migratory expression profile of cell-bound AM is altered by GA treatment. While this alteration may contribute to the beneficial action of the drug, the prolonged development and unselective changes indicate more secondary immune regulatory phenomena related to these effects.
ICAM= adhesion molecule so is LFA-1 and VLA-4 (integrins) and the selectins some of them go down abit after treatment so they may not bind to antigen presenting cells as well as they could and maybe also may bind less to blood vessels in the brain. What else doesn't GA do?