For instance, a previous study revealed that the progression of experimental autoimmune uveitis was regulated by both HVEM-LIGHT and HVEM-BTLA interactions for HVEM-mediated stimulatory signaling, while another study described a protective role of HVEM-BTLA interactions in suppressing T cell-mediated responses to reduce the severity of experimental autoimmune encephalomyelitis (20, –, 22). This evidence concerns the gene TNFRSF14 and experimental autoimmune encephalomyelitis.