@article{3f8551f908d94a0a8ec68aea70e52dd5,
title = "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.",
author = "Yuwen Zhu and Sheng Yao and Augustine, {Mathew M.} and Haiying Xu and Jun Wang and Jingwei Sun and Megan Broadwater and William Ruff and Liqun Luo and Gefeng Zhu and Koji Tamada and Lieping Chen",
note = "Funding Information: Female C57BL/6 mice aged 6 to 10 weeks were purchased from the National Cancer Institute, National Institutes of Health (NIH) (Frederick, MD). The HVEM−/− mice with a C57BL/6 background have been pre- viously described and were provided by W. W. Hancock (37). All fusion proteins were generated by fusing the extracellular domain of each molecule with either mouse or human Fc tags (38). Hamster mAbs against mSALM5 were generated by immunizing a hamster with mSALM5-Ig fusion protein. All antibodies for flow cytometry staining, if not specified, were purchased from BD Biosciences or eBioscience. Publisher Copyright: {\textcopyright} 2016 The Authors.",
year = "2016",
month = apr,
doi = "10.1126/sciadv.1500637",
language = "English (US)",
volume = "2",
journal = "Science advances",
issn = "2375-2548",
publisher = "American Association for the Advancement of Science",
number = "4",
}