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

ABSTRACT: 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.

SUBMITTER: Zhu Y 

PROVIDER: S-EPMC4846428 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature

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

Zhu Yuwen Y   Yao Sheng S   Augustine Mathew M MM   Xu Haiying H   Wang Jun J   Sun Jingwei J   Broadwater Megan M   Ruff William W   Luo Liqun L   Zhu Gefeng G   Tamada Koji K   Chen Lieping L  

Science advances 20160408 4

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 inflam  ...[more]