This is very interesting. Copaxone is a popular drug that is used to treat multiple sclerosis. This is a drug that essentially incude the parts of a myelin protein called myelin basic protein (MBP). In theory, this treatment seems to be contradictory. It is like a vaccine that stimulates the immune system to attack a myelin protein. However, it was shown in both animal and human studies to reduce the progressive immune damage to myelin. This study suggets that it causes apoptosis or programmed cell death in lymphocytes, the cells of the immune system. Wise.

[*] Ruggieri M, Avolio C, Scacco S, Pica C, Lia A, Zimatore GB, Papa S, Livrea P and Trojano M (2005). Glatiramer acetate induces pro-apoptotic mechanisms involving Bcl-2, Bax and Cyt-c in peripheral lymphocytes from multiple sclerosis patients. J Neurol Apoptotic deletion of autoreactive T-cells is defective in patients with multiple sclerosis (MS). Glatiramer acetate (GA) treatment seems to restore apoptosis of detrimental T-cells. We analyzed the mitochondria membrane pro- (Bax) and anti-apoptotic (Bcl- 2) and cytosolic pro-apoptotic (Cyt-c, APAF-1) proteins expression in peripheral lymphocytes from relapsing-remitting (RR) MS patients during GA treatment. Blood samples were collected from 8 healthy controls (HCs) and from 8 RR MS patients prior to and every three months during the 9 months of GA treatment. Peripheral blood mononuclear cells (PBMNCs) Bcl-2, Bax, Cyt-c and APAF-1 were quantified by western blot followed by densitometric scanning and Bax/Bcl-2, cytosolic Cyt-c/Bcl-2 and APAF-1/Bcl-2 ratios were calculated. T-cells were in vitro tested for oxygen consumption by a respirometric analysis. Bax/Bcl-2, cytosolic Cyt-c/Bcl-2 and APAF-1/Bcl-2 ratios in untreated MS patients were significantly (p < 0.05) lower than in HCs. Bax/Bcl-2 ratio increased (p = 0.03) and Cyt-c/Bcl-2 ratio showed a trend to increase during the 9 months of GA treatment in MS patients. A reduction of 58% and 59% in oxygen consumption by PBMNCs was evident after GA treatment in vitro or when GA treated patients' cells were compared with those from HCs, respectively. Our findings suggest that GA exerts a regulatory effect on peripheral T lymphocytes through pro-apoptosis mechanisms involving mitochondria and cytosolic proteins. Dept. of Neurological and Psychiatric Sciences, University of Bari, Policlinico, Piazza Giulio Cesare, 70124, Bari, Italy, mruggieri@neurol.uniba.it. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16184340