The major findings in the present study are that: 1) endogenous type I IFN-like activity and treatment with IFN-β are both associated with reduced expression of CD49d on CD26high CD4+ T cells (Th1 helper cells) and this correlates with MRI disease activity in IFN-β-treated MS patients; 2) treatment with IFN-β also induces activation of CD4+ T cells, as evidenced by the induction of CD71 and HLA-DR, and this is associated with an increased relapse risk. This evidence concerns the gene ITGA4 and myeloid sarcoma.