Claudin-11 contributed to the formation of strong TJs, and the expression of claudin-11 was downregulated in the brain and spinal cord capillaries of experimental autoimmune encephalomyelitis (EAE) model mice, widely used as an animal model of CNS inflammation multiple sclerosis, and in patients with multiple sclerosis [34,35]. Here, CLDN11 is linked to experimental autoimmune encephalomyelitis.