Effect of glatiramer acetate (Copaxone ®) on the immunophenotypic and cytokine profile and BDNF production in multiple sclerosis: A longitudinal study

• Published in: Neuroscience letters Vol. 406; no. 3; pp. 270 - 275
• Main Authors: Blanco, Y., Moral, E.A., Costa, M., Gómez-Choco, M., Torres-Peraza, J.F., Alonso-Magdalena, L., Alberch, J., Jaraquemada, D., Arbizu, T., Graus, F., Saiz, A.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 09-10-2006; Elsevier
• Subjects: Adjuvants, Immunologic - pharmacology; Adjuvants, Immunologic - therapeutic use; Adult; BDNF; Biological and medical sciences; Brain-Derived Neurotrophic Factor - metabolism; Cytokines; Cytokines - metabolism; Female; Flow Cytometry - methods; Fundamental and applied biological sciences. Psychology; Glatiramer Acetate; Humans; Immunomodulatory treatment; Longitudinal Studies; Lymphocyte Activation - drug effects; Lymphocyte immunophenotyping; Male; Medical sciences; Middle Aged; Multiple sclerosis; Multiple Sclerosis - drug therapy; Multiple Sclerosis - immunology; Multiple Sclerosis - metabolism; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Neurology; Peptides - pharmacology; Peptides - therapeutic use; T-Lymphocyte Subsets - drug effects; Time Factors; Vertebrates: nervous system and sense organs; Glatiramer acetate; Lymphocyte immunophenotyping; Immunomodulatory treatment; Multiple sclerosis; Cytokines; BDNF; Nervous system diseases; Cytokine; Inflammatory disease; Treatment; Follow up study; Central nervous system disease; Brain derived neurotrophic factor; Lymphocyte
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2006.07.043

We assessed the effect of glatiramer acetate (GA) on the immunophenotypic and cytokine profile and the BDNF production by peripheral blood mononuclear cells, and their association with the clinical response in 19
naïve-treated MS patients prospectively followed-up after GA therapy. Two patients withdrew the therapy. After a median follow-up of 21 months, twelve were considered responders and five as non-responders. Non-responder patients had significant longer disease duration and a higher EDSS score at baseline. In the responder group, a significant decrease in the percentage of INF-γ producing total lymphocytes, CD4
+ and CD8
+ T cells, and reduced percentage of IL-2 producing CD4
+ and CD8
+ T cells were observed at 12, 18 and 24 months. These changes were associated with a significant increase in the percentage of CD3
+, CD4
+ and CD4
+CD45RA
+ T cells, and BDNF production from month 6 that remained significant throughout the study. We did not observe significant changes in the nonresponder group for any of the parameters studied. Our data suggest that GA treatment induces a downmodulation of proinflammatory cytokines associated with the regulation of the peripheral T cell compartment and with increased production of BDNF that might be related to the clinical response.