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Sci Adv. 2016 Apr 8;2(4):e1500637. doi: 10.1126/sciadv.1500637. eCollection 2016 Apr.

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

Author information

1
Department of Immunobiology, Yale School of Medicine, New Haven, CT 06520, USA.
2
Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
3
Department of Immunobiology, Yale School of Medicine, New Haven, CT 06520, USA.; Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.

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.

KEYWORDS:

BBB; CNS; SALM5; immune privilege

PMID:
27152329
PMCID:
PMC4846428
DOI:
10.1126/sciadv.1500637
[Indexed for MEDLINE]
Free PMC Article

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