Carboplatin ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by inducing T cell apoptosis.

Apoptosis is a natural physiological process that can maintain the homeostasis of the body and immune system. This process plays an important role in the system's resistance to autoimmune development. Because of the dysfunction of cell apoptosis mechanism, the number of autoreactive cells in the peripheral tissue increases along with their accumulation. This will lead to the development of autoimmune diseases, such as multiple sclerosis (MS). MS is an immune-mediated disease of the central nervous system characterized by severe white matter demyelination. Because of the complexity of its pathogenesis, there is no drug to cure it completely. Experimental autoimmune encephalomyelitis (EAE) is an ideal animal model for the study of MS. Carboplatin (CA) is a second-generation platinum anti-tumor drug. In this study, we attempted to assess whether CA could be used to ameliorate EAE. CA reduced spinal cord inflammation, demyelination, and disease scores in mice with EAE. Moreover, the number and proportion of pathogenic T cells especially Th1 and Th17 in the spleen and draining lymph nodes were reduced in CA-treated EAE mice. Proteomic differential enrichment analysis showed that the proteins related to apoptosis signal changed significantly after CA treatment. CFSE experiment showed that CA significantly inhibited the T cell proliferation. Finally, CA also induced apoptosis in activated T cells and MOG-specific T cells in vitro. Overall, our findings indicated that CA plays a protective role in the initiation and progression of EAE and has the potential to be a novel drug in the treatment of MS.