Multiple sclerosis (MS) is the most common autoimmune disease of the central nervous system and is one of the foremost causes of nontraumatic neurological disability in young adults. Researchers discovered Aurintricarboxylic acid (ATA) significantly alleviated the clinical symptoms of EAE, a mouse model of MS. ATA has been reported to inhibit ribonuclease and topoisomerase II by preventing the binding of the nucleic acid to the enzyme; and to inhibit viral reproduction and infection. It has been used to inhibit protein biosynthesis in biological experiments, and as an ammonium salt (aluminon), it is used as a reagent to detect aluminium in various samples.

Researchers discovered though ATA treatment significantly reduces the clinical score of EAE, it does not directly inhibit the differentiation of Th1 and Th17 cells in vitro. ATA was found to block the chemotaxis and accumulation of dendritic cells in the spleen of EAE mice before the onset of the disease, and reduce the differentiation of Th1 and Th17 cells in the spleen. Further study revealed that ATA also blocks the infiltration of pathogenic T cells into the CNS and block the onset of passive EAE. ATA was found to inhibit the functions of many chemokine receptors. By blocking chemokine mediated migration of dendritic cells and pathogenic T cells, ATA alleviates the pathogenesis of EAE and might be used to treat autoimmune diseases including multiple sclerosis.These results were recently published in the Journal of Immunology (2012/12/24 online).

This work was directed by Dr. XIE Xin, a Principle Investigator of SIMM (Shanghai Institute of Materia Medica, CAS), the deputy director of the National Center for Drug Screening, and an Adjunct Professor of Tongji University. Her research is mainly focused on GPCR-based drug discovery and chemical biology of stem cells. Her group recently reported that drugs targeting CysLT1 receptor or A2B adenosine receptor might be used to treat MS (Journal of Immunology. 2011,187:2336-45; Journal of Immunology. 2013, Jan 1;190(1):138-46).

This work was supported by grants from the Chinese Academy of Sciences, the National Natural Science Foundation of China, Ministry of Science and Technology of China, and Shanghai Commission of Science and Technology.

Original Article：http://www.jimmunol.org/content/early/2012/12/24/jimmunol.1201994.long

　　Figure: A, ATA alleviates EAE in a dose-dependent way; B, ATA reduces the percentage of dendritic cells, Th1 and Th17 cells in spleen of EAE mice; C, ATA inhibits the homing of dendritic cells; D, ATA blocks chemokine mediated migration of dendritic cells; E, ATA inhibits passive EAE; F, ATA reduces pathogenic cell infiltration into the CNS; G, ATA blocks the functions of chemokine receptors but not other GPCRs.