Neuron-specific SALM5 limits inflammation in the CNS via its interaction with HVEM

Yuwen Zhu, Sheng Yao, Mathew M. Augustine, Haiying Xu, Jun Wang, Jingwei Sun, Megan Broadwater, William Ruff, Liqun Luo, Gefeng Zhu, Koji Tamada, Lieping Chen

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


The central nervous system (CNS) is an immune-privileged organ with the capacity to prevent excessive inflammation. Aside from the blood-brain barrier, active immunosuppressive mechanisms remain largely unknown. We report that a neuron-specific molecule, synaptic adhesion-like molecule 5 (SALM5), is a crucial contributor to CNS immune privilege. We found that SALM5 suppressed lipopolysaccharide-induced inflammatory responses in the CNS and that a SALM-specific monoclonal antibody promoted inflammation in the CNS, and thereby aggravated clinical symptoms of mouse experimental autoimmune encephalomyelitis. In addition, we identified herpes virus entry mediator as a functional receptor that mediates SALM5's suppressive function. Our findings reveal a molecular link between the neuronal system and the immune system, and provide potential therapeutic targets for the control of CNS diseases.

Original languageEnglish (US)
Article numbere1500637
JournalScience Advances
Issue number4
StatePublished - Apr 2016

ASJC Scopus subject areas

  • General


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