Antithyroid drugs (thionamides such as carbimazole and its active metabolite methimazole, and propyl thiouracile) are taken up by the thyroid gland just as the other anions similar to iodide (perchlorate, thiocyanate, pertechnetate). Their target is the thyroid peroxidase. They block the iodation of tyrosine residues and the coupling of iodotyrosines into iodothyronines. However, beyond the inhibition of thyroid hormone synthesis, antithyroid drugs appear to have the capacity of interfering with the immunological abnormalities involved in Graves' hyperthyroidism: they cure 50% of the patients provided they are maintained for at least 12 months and they significantly decrease the titers of antithyroid antibodies in most of the patients. Potential immunomodulatory effects of antithyroid drugs seem to involve thyroid depletion of iodine which might reduce antigen expression, and scavenging of reactive free radicals generated from oxygen and/or iodide during peroxidation. A direct toxic effect of thionamides on immuno-competent cells seems unlikely. Whatever the mechanisms, more accurate elucidation of the immunomodulatory action of antithyroid drugs might contribute to a better understanding of the thyroid-immune derangements involved in the initiation or perpetuation of Graves' hyperthyroidism.