Draft:CAR Treg therapy in multiple sclerosis

== Preclinical Translation ==

== Preclinical Translation ==

Preclinical studies using the [[experimental autoimmune encephalomyelitis]] ([[Experimental autoimmune encephalomyelitis|EAE]]) model have shown the efficacy of CAR-Treg therapy in reducing [[neuroinflammation]] and disease severity. [[In vitro]], CAR-Tregs exhibit strong immunosuppressive activity. In vivo, they reduce disease symptoms, prevent relapses, and suppress [[demyelination]]. CAR-Tregs engineered to recognize [[Myelin oligodendrocyte glycoprotein|MOG]] were able to migrate to the [[Central nervous system|CNS]] after intranasal administration, inhibit autoreactive T cells' proliferation, and reduce the production of [[proinflammatory cytokines]] in EAE mice. Overall, these results support CAR-Tregs as a promising therapeutic approach in MS. However, they remain at the preclinical stage, with no proven clinical benefit in humans so far.

Preclinical studies using the [[experimental autoimmune encephalomyelitis]] ([[Experimental autoimmune encephalomyelitis|EAE]]) model have shown the efficacy of CAR-Treg therapy in reducing [[neuroinflammation]] and disease severity. [[In vitro]], CAR-Tregs exhibit strong immunosuppressive activity. In vivo, they reduce disease symptoms, prevent relapses, and suppress [[demyelination]]. CAR-Tregs engineered to recognize [[Myelin oligodendrocyte glycoprotein|MOG]] were able to migrate to the [[Central nervous system|CNS]] after intranasal administration, inhibit autoreactive T cells' proliferation, and reduce the production of [[proinflammatory cytokines]] in EAE mice. Overall, these results support CAR-Tregs as a promising therapeutic approach in MS. However, they remain at the [[preclinical]] stage, with no proven clinical benefit in humans so far.

== Challenges and limitations ==

== Challenges and limitations ==