Abstract
We recently showed that B cells reduce CNS inflammation in mice with experimental allergic encephalomyelitis (EAE). Here, we demonstrate that adoptively transferred CD5/CD19+ B cells protect against EAE severity. Furthermore, we show that glatiramer acetate (GA), a therapeutic for relapsing multiple sclerosis treatment, amplifies this effect. Transfer of GA-conditioned B cells leads to increased production of immunoregulatory cytokines and reduced CNS inflammation, as well as decreased expression of the chemokine receptor, CXCR5, and elevated BDNF expression in the CNS. Thus B cells can protect against EAE, and GA augments this effect in maintaining immune homeostasis and controlling EAE disease progression.
Copyright © 2010 Elsevier B.V. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adoptive Transfer
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Animals
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Antigens, CD19 / immunology
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Antigens, CD19 / metabolism
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B-Lymphocyte Subsets / drug effects*
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B-Lymphocyte Subsets / immunology*
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B-Lymphocyte Subsets / metabolism
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Brain-Derived Neurotrophic Factor / biosynthesis
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Brain-Derived Neurotrophic Factor / drug effects
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CD5 Antigens / immunology
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CD5 Antigens / metabolism
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Cell Separation
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Encephalomyelitis, Autoimmune, Experimental / metabolism
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Encephalomyelitis, Autoimmune, Experimental / pathology
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Female
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Flow Cytometry
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Glatiramer Acetate
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Immunosuppressive Agents / pharmacology*
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Mice
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Mice, Inbred C57BL
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Peptides / pharmacology*
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Receptors, CXCR5 / biosynthesis
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Receptors, CXCR5 / drug effects
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Reverse Transcriptase Polymerase Chain Reaction
Substances
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Antigens, CD19
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Brain-Derived Neurotrophic Factor
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CD5 Antigens
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CXCR5 protein, mouse
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Immunosuppressive Agents
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Peptides
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Receptors, CXCR5
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Glatiramer Acetate