Termination of inflammation in the nervous system

R. Gold, R. A. Linker, A. Chan

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


T cell apoptosis has been studied in animal models for human autoimmune disorders of the nervous system and in other tissues devoid of specialized immune-defense mechanisms. Our data suggest that the central nervous system has a high potential to eliminate T cell inflammation, whereas this mechanism is less effective in the peripheral nervous system, and even more in muscle and skin. In-vitro experiments indicate different scenarios how specific cellular and humoral elements in the nervous system may synergize and sensitize T cells for apoptosis in-vivo. Probably release of TNF-alpha in the nervous system is a central mechanism to limit inflammation in the brain. This is further substantiated since neutralization of TNF-alpha in MS patients increased cellular inflammation and relapses. Therapeutically several conventional and novel approaches like glucocorticosteroids and high-dose antigen therapy induce T cell apoptosis in-situ. We also discuss regulatory, proapoptotic mechanisms such as the Fas/FasL system and counterregulatory mechanisms that have been utilized to limit tissue damage.

Original languageEnglish
Pages (from-to)672-676
Number of pages5
JournalRevue Neurologique
Issue number6-7
StatePublished - Jun 2007
Externally publishedYes


  • Apoptosis
  • Experimental autoimmune encephalomyelitis
  • Fas
  • TNF


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