CONCLUSION:Our data suggest that there is no general immune deficiency in non-/low-responders. Thus, we hypothesize that the induction of anti-HBsAg responses by vaccination is significantly dependent on the pre-existing T cell repertoire against the specific antigen rather than the presence of a general T cell defect. INTRODUCTIONWorldwide, hepatitis B virus (HBV) infections are a growing problem with a high prevalence of over 8% hepatitis B surface antigen (HBsAg) positive individuals in Africa, South America, parts of Eastern Europe, South Asia, and Canada [1] . It is estimated that approximately 350 million people are chronic carriers of HBV with 1-1.5 million dying from liver cirrhosis and primary liver cancer [2] . Nowadays, protective repeated vaccinations with recombinant HBsAg are not only recommended to all health care workers and travellers, but have recently been included in the childhood and adolescence immunization schedule. Hepatitis B vaccinations prevent HBV infections as well as its complications in most of the vaccines [3,4] . However, 5% to 10% fail to produce protective anti-HBsAg titers after three vaccinations irrespective of the source of the antigen, which is a problem not only for health care workers, and represents a major medical as well as economic challenge [5][6][7] . Low-(HBsAg titer 10-99 kU/L) or Abstract AIM: To evaluate, whether humoral hepatitis-B-vaccine non-responders also fail to mount a T cell response and to compare these results to normal vaccines. RAPID COMMUNICATION T cell responses to hepatitis B surface antigen are detectable in non-vaccinated individuals