Background. The underlying mechanisms that lead to the development of the chronic HBsAg carrier state are not known. Host cellular and humoral immune responses are suspected of being important. Thus the chronic carrier state is particularly common amo...
Background. The underlying mechanisms that lead to the development of the chronic HBsAg carrier state are not known. Host cellular and humoral immune responses are suspected of being important. Thus the chronic carrier state is particularly common among individuals with conditions or diseases associated with significant immunologic hyporesponsiveness such as uremia, Down s syndrome, leukemia and leprosy. Methods. In vitro T cell proliferative responses to phytohemagglutinin(PHA), mitogenic anti-CD3 monoclonal antibody and mitogenic combination of anti-CD2 9-1 and 9.6 and mitogen-induced interleukin-2(IL-2) and 2'5'-oligoadenylate synthetase (2'5'-AS) production were studied in 7 asymptomatic uremic HBsAg carriers (UC), 11 non-uremic asymptomatic carriers (NC), 6 uremic responders (1JR) and 12 non-uremic responders (NR) to hepatitis B vaccine in order to study immune responses of uremic HBsAg carriers. Peripheral blood mononuclear cells (PBMC) were separated by Ficoll-Hypaque gradient centrifugation. IL-2 production was measured by ELISA method and 2'5'-AS by RIA. Results. 1) The number of circulating lymphocytes was significantly lower in UC than in NR and NC. 2) Proliferative responses of PBMC from UC were not different from those of NR, NC, and UR. 3) IL-2 production was significantly higher in PHA- stimulated than in unstimualted cultures in all 4 groups but was most prominent in UR. Both unstimulated and stimulated IL-2 production were highter in NC, UR, and UC than in NR. 4) 2'5'-AS production was significantly greater in PHA-stimulated than in unstimulated cultures in all 4 groups but was significantly lower in UC than in NR or UR. No difference was observed between NC and UC. Conclusion. It appears that the defect in interferon production may play an important role in the development and maintenance of chronic HBsAg carrier state in uremia.