Accelerated central nervous system autoimmunity in BAFF-receptor-deficient mice

作者：Kim Susan S^*; Richman David P; Zamvil Scott S; Agius Mark A

来源：Journal of the Neurological Sciences, 2011, 306(1-2): 9-15.

DOI：10.1016/j.jns.2011.04.008

• B-cell activating factor
• BAFF-receptor
• Experimental autoimmune encephalomyelitis
• Multiple sclerosis
• Central nervous system inflammation
• Macrophages
• T-cells

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.

• 出版日期2011-7-15