The role of collapsin response mediator protein 2 in multiple sclerosis-related T cell functions

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system(CNS)in which T cells play an important role. A proteomics study illustrated the differential expression of collapsin response mediator protein 2 (CRMP2) in the animal model of MS. Additionally, literature showed that phosphorylated CRMP2 is present in chronic MS lesions and that a higher expression of CRMP2 in peripheral T cells correlates with a higher migration of these cells into the CNS. We hypothesized that a knockdown of CRMP2 results in an altered migration and differentiation of T cells, which could improve the clinical outcome in MS and in its animal model. Because T cells are difficult to transfect, we needed to optimize the transfection efficiency. This was the highest when activated Jurkat T cells were transfected using TransFectin in serum-reduced conditions. Next, a knockdown of CRMP2 was established 120 and 144 hours after transfection. The T cell properties could not be investigated.