Journal
IMMUNITY
Volume 43, Issue 6, Pages 1174-1185Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.10.017
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Funding
- Japan Society for Promotion of Science (JSPS) [15H05703]
- JSPS [26713015, 15H05653]
- grant for the ERATO Takayanagi Osteonetwork Project from JST
- Japan Agency for Medical Research and Development [15ek0109106]
- Era of Hope
- ERC
- grant for PRESTO from JST
- [22-00131]
- Grants-in-Aid for Scientific Research [15F15414, 26713015, 15K15149, 15H05653, 15H05703] Funding Source: KAKEN
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The central nervous system (CNS) is an immunologically privileged site protected from uncontrolled access of T cells by the blood-brain barrier (BBB), which is breached upon autoimmune inflammation. Here we have shown that receptor activator of nuclear factor-kappa B (NF-kappa B) ligand (RANKL) on T cells regulates C-C type chemokine ligand 20 (CCL20) production by astrocytes and T cell localization in the CNS. Importantly, mice specifically lacking RANKL in T cells were resistant to experimental autoimmune encephalomyelitis (EAE) due to altered T cell trafficking. Pharmacological inhibition of RANKL prevented the development of EAE without affecting the peripheral immune response, indicating that RANKL is a potential therapeutic target for treating autoimmune diseases in the CNS.
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