| First Author | Zhu Y | Year | 2016 |
| Journal | Sci Adv | Volume | 2 |
| Issue | 4 | Pages | e1500637 |
| PubMed ID | 27152329 | Mgi Jnum | J:258189 |
| Mgi Id | MGI:6140757 | Doi | 10.1126/sciadv.1500637 |
| Citation | Zhu Y, et al. (2016) Neuron-specific SALM5 limits inflammation in the CNS via its interaction with HVEM. Sci Adv 2(4):e1500637 |
| abstractText | 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. |
