Increased expression of B cell-associated regulatory cytokines by glatiramer acetate in mice with experimental autoimmune encephalomyelitis

• Published in: Journal of neuroimmunology 2010-02, Vol.219 (1), p.47-53
• Main Authors: Begum-Haque, Sakhina, Sharma, Alok, Christy, Marc, Lentini, Tim, Ochoa-Reparaz, Javier, Fayed, Islam F, Mielcarz, Daniel, Haque, Azizul, Kasper, Lloyd H
• Format: Article
• Language: English
• Subjects: A proliferation-inducing ligand (APRIL); Allergy and Immunology; Animals; Antigens, CD19 - metabolism; B cell-activating factor (BAFF); B-Cell Activating Factor - genetics; B-Cell Activating Factor - metabolism; B-Lymphocytes - drug effects; Brain - pathology; CD5 Antigens - metabolism; Cells, Cultured; Cytokines - genetics; Cytokines - metabolism; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental - chemically induced; Encephalomyelitis, Autoimmune, Experimental - drug therapy; Encephalomyelitis, Autoimmune, Experimental - pathology; Experimental autoimmune encephalomyelitis (EAE); Female; Flow Cytometry - methods; Gene Expression Regulation - drug effects; Glatiramer Acetate; Glatiramer Acetate (GA); Glycoproteins; IL-13 production; Immunosuppressive Agents - pharmacology; Immunosuppressive Agents - therapeutic use; Lymph Nodes - pathology; Mice; Mice, Inbred C57BL; Myelin-Oligodendrocyte Glycoprotein; Neurology; Peptide Fragments; Peptides - pharmacology; Peptides - therapeutic use; RNA, Messenger - metabolism; Spleen - pathology; Tumor Necrosis Factor Ligand Superfamily Member 13 - genetics; Tumor Necrosis Factor Ligand Superfamily Member 13 - metabolism
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/j.jneuroim.2009.11.016

Abstract B cells are of increasing importance as a target for multiple sclerosis treatment. Here we show that GA treatment of mice with experimental autoimmune encephalomyelitis (EAE) biases cytokine production by B cells towards cytokines associated with regulation in MS including interleukin (IL)-4, -10 and -13 and reduces pro-inflammatory IL-6, IL-12, and TNF alpha levels. GA also down-regulates expression of B cell-activating factor (BAFF) of the TNF family and a proliferation-inducing ligand (APRIL), as well as the BAFF receptor in mice with EAE. Thus, GA impacts both B cell survival and B cell cytokine production during CNS inflammatory disease in an EAE model.