In experimental autoimmune encephalomyelitis (EAE, a murine model of multiple sclerosis) the production of GM-CSF by CD4+ T cells is necessary and sufficient to render them encephalitogenic.27, 28 GM-CSF is thought to exert its pathogenic effect in this model by enhancing IL-23 production by CNS-infiltrating CD11c+ DCs and thereby stabilising the Th17 population.27 In RA synovial tissue CD4+ T cells colocalise with CD1c+ DCs29 suggesting a potential symbiotic interaction which promotes inflammation. The gene discussed is CD4; the disease is experimental autoimmune encephalomyelitis.