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

被引：24

作者：

Kim, Susan S. ^{[1
,2
]}

Richman, David P. ^{[1
,2
]}

Zamvil, Scott S. ^{[3
,4
]}

Agius, Mark A. ^{[1
,2
,5
]}

机构：

[1] Univ Calif Davis, Dept Neurol, Davis, CA 95616 USA

[2] Univ Calif Davis, Neurosci Grad Program, Davis, CA 95616 USA

[3] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA

[4] Univ Calif San Francisco, Program Immunol, San Francisco, CA USA

[5] Vet Adm No Calif Hlth Care Syst, Mather, CA USA

来源：

JOURNAL OF THE NEUROLOGICAL SCIENCES | 2011年 / 306卷 / 1-2期

关键词：

B-cell activating factor; BAFF-receptor; Experimental autoimmune encephalomyelitis; Multiple sclerosis; Central nervous system inflammation; Macrophages; T-cells; B-CELL; MULTIPLE-SCLEROSIS; T-CELL; A/WYSNJ MICE; DISEASE; ACTIVATION; ENCEPHALOMYELITIS; BCMA;

D O I：

10.1016/j.jns.2011.04.008

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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.

引用

页码：9 / 15

页数：7

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