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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-κB (NF-κB) 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.

Original publication




Journal article



Publication Date





1174 - 1185


Animals, Astrocytes, Chemotaxis, Leukocyte, Coculture Techniques, Encephalomyelitis, Autoimmune, Experimental, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Immunohistochemistry, Lymphocyte Activation, Mice, Mice, Knockout, RANK Ligand, Real-Time Polymerase Chain Reaction, T-Lymphocytes