Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1914182 | Journal of the Neurological Sciences | 2011 | 7 Pages |
Abstract
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.
Keywords
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Ageing
Authors
Susan S. Kim, David P. Richman, Scott S. Zamvil, Mark A. Agius,