During experimental autoimmune encephalomyelitis (EAE), CX3CR1 deficiency confers exacerbated disease defined by severe inflammation and neuronal loss.
In addition, we showed that the enzyme tissue transglutaminase (TG2), which is present in CNS-infiltrated cells in MS patients, is likewise found in CX3CR1-GFP<sup>+</sup> monocytes in the spinal cord lesions and at the luminal side of the vasculature during EAE.
This is the first study to identify CX3CL1 signaling through CX3CR1 via the DRG/SC anatomical connection that represents a critical pathway involved in NPP induction in an EAE model of MS.
Induction of experimental allergic encephalomyelitis (EAE) in the rat was accompanied by increased levels of CCR2, CCR5, CXCR4, and CX3CR1 mRNAs in the lumbar spinal cords of animals displaying clinical signs of the disease.