Amelioration of experimental autoimmune encephalomyelitis by clozapine is not associated with defective CD4 T cell responses

Pirooz Zareie, Bronwen Connor, Anne Camille La Flamme

Research output: Contribution to journalArticleResearchpeer-review

6 Citations (Scopus)


Atypical antipsychotic agents, such as clozapine, are used for treating psychosis and depression and have recently been found to modulate neuroinflammation. We have shown previously that treatment of mice with the atypical antipsychotic agents, clozapine or risperidone, attenuates disease severity in experimental autoimmune encephalomyelitis (EAE); however, the mechanism by which they are protective is unknown. In this study, we investigated the effects of clozapine on CD4+ T cell responses and found that clozapine did not significantly affect the expansion of myelin-specific T cells, their differentiation into pathogenic subsets, or their encephalitogenic capacity to induce EAE. Interestingly, although clozapine enhanced differentiation of regulatory T (Treg) cells, in vivo neutralization of Tregs indicated that Tregs were not responsible for the protective effects of clozapine during the induction and effector phase of EAE. Taken together, our studies indicate that clozapine does not mediate its protective effects by directly altering CD4 T cells.

Original languageEnglish
Article number68
Number of pages10
JournalJournal of Neuroinflammation
Issue number1
Publication statusPublished - 29 Mar 2017
Externally publishedYes


  • Atypical antipsychotics
  • EAE
  • MS
  • Neuroinflammation

Cite this