Tumour necrosis factor-α (TNF-α) plays a central role in inflammatory events including those
taking place in the central nervous system (CNS), and has been implicated as a key
pathogenicc mediator in several human inflammatory, infectious and autoimmune CNS
disorders. Using transgenic and gene knockout mice we have investigated the role of
deregulated TNF-α production in the CNS. We show that the overexpression of wild-type
murine or human TNF-α transgenes by resident CNS astrocytes or neurons in sufficient to …