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The Journal of Neuroscience, May 13, 2009, 29(19):6348-6352; doi:10.1523/JNEUROSCI.5040-08.2009

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Brief Communications
Identification of BLyS (B Lymphocyte Stimulator), a Non-Myelin-Associated Protein, as a Functional Ligand for Nogo-66 Receptor

Lei Zhang,^1,2 Sushuang Zheng,¹ Haitao Wu,³ Yan Wu,³ Shuhong Liu,³ Ming Fan,³ and Jian Zhang¹

¹Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, the Chinese Academy of Sciences, Beijing 100101, China, ²Graduate School of the Chinese Academy of Sciences, Beijing 100039, China, and ³Department of Neurophysiology, Institute of Basic Medical Sciences, Beijing 100850, China

Correspondence should be addressed to Dr. Jian Zhang, Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, the Chinese Academy of Sciences, Beijing 100101, China. Email: jianzhang84{at}genetics.ac.cn

B lymphocyte stimulator (BLyS), a tumor necrosis factor family protein essential for B cell development, was previously shown to be expressed at an elevated level in the CNS of multiple sclerosis patients. Although it may be involved in CNS diseases, its exact functions in CNS remain unknown. We hypothesize that BLyS may be a negative regulator for neuronal functions. Here Nogo-66 receptor (NgR) is identified as a high affinity receptor for BLyS, which inhibits dorsal root ganglion outgrowth in culture. The inhibition by BLyS can be reversed by a truncated NgR or by removal of glycosylphosphatidylinositol-linked proteins from neurons. More importantly, the inhibitory effect by BLyS is significantly diminished for neurons isolated from NgR^–/– mice. Furthermore, expressions of BLyS and NgR are also found to be associated with astrocytes and macrophages/microglial cells at spinal cord injury sites. Thus, BLyS can function independently of myelin-associated inhibitors and likely serves as a redundant NgR ligand that negatively influences axonal outgrowth in CNS.

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Received Oct. 18, 2008; revised March 28, 2009; accepted April 13, 2009.

Correspondence should be addressed to Dr. Jian Zhang, Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, the Chinese Academy of Sciences, Beijing 100101, China. Email: jianzhang84{at}genetics.ac.cn

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