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
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Article info
Publication history
Published online: April 29, 2011
Accepted:
April 4,
2011
Received in revised form:
April 2,
2011
Received:
December 16,
2010
Identification
Copyright
Published by Elsevier Inc.
