Concordance and contradiction concerning cytokines and chemokines in experimental demyelinating disease

Abstract

Experimental autoimmune encephalomyelitis (EAE) has served as a model for human demyelinating diseases, including multiple sclerosis. EAE is mediated by CD4+ T lymphocytes of the TH1 subset. These T cells produce inflammatory cytokines and chemokines that are associated with pathogenicity. The disease is downregulated by other T cells, presumably of the TH2 subset that secrete a different pattern of cytokines which modulate the activity of the pathogenic TH1 cells. Ongoing studies should provide insight into how the interactions of T-cell subsets impact on the pathogenesis of autoimmune demyelinating diseases.