THE presence of hepatitis B surface antigen (HBsAg) in blood is a marker of infection with hepatitis B virus (HBV). Persistence of the antigen in the blood of 'carriers' is a manifestation of proliferation of HBV in liver cells and this carrier state can be associated with various types of liver disease1. In guinea pigs and chimpanzees, immunisation with HB sAg in Freund's complete adjuvant (FCA) elicits a cutaneous delayed type hypersensitivity (DTH) response2,3. It is believed that integrity of the thymus-dependent cell-mediated immune system in man is necessary for resistance to HBV, and that deficiency of cell-mediated immunity could predispose to development of the carrier state4,5. We therefore investigated the contribution of thymus-derived cells to the immune response to HBsAg in mice by immunisation of BALB/c mice, mice heterozygous for the nude mutant gene (nu/+), and congenitally athymic mice of the nu/nu strain, using purified HBsAg.