Journal
JOURNAL OF THE NEUROLOGICAL SCIENCES
Volume 306, Issue 1-2, Pages 9-15Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jns.2011.04.008
Keywords
B-cell activating factor; BAFF-receptor; Experimental autoimmune encephalomyelitis; Multiple sclerosis; Central nervous system inflammation; Macrophages; T-cells
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Funding
- University of California
- National Institute of Health (NIH) [RO1 AI073737, RO1 AI059709, RO1 NS063008]
- National Multiple Sclerosis Society (NMSS) [RG 3622, 3913]
- Dana Foundation
- Guthy Jackson Charitable Foundation
- Maisin Foundation
- California Myasthenia Gravis Foundation
- TEVA Neuroscience
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B cell activating factor (BAFF) is critical for B cell survival, a function that is mediated by BAFF receptor, (BAFF-R). The role of BAFF (or BAFF-R) in the multiple sclerosis model, experimental autoimmune encephalomyelitis (EAE), was examined using BAFF-R-deficient mice. BAFF-R deficiency resulted in paradoxically increased severity of EAE induced by myelin-oligodendrocyte glycoprotein (MOG) peptide 35-55. Inflammatory foci in BAFF-R-deficient mice comprised increased numbers of activated macrophages expressing BAFF and correlated with increased BAFF secretion. Thus, BAFF-R may be important in EAE pathogenesis, possibly by influencing macrophage function through a mechanism that involves modulation of BAFF expression. Published by Elsevier B.V.
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