ABSTRACT
A proportion of healthy neonates and adults fail to develop a protective antibody response to recombinant hepatitis B [HB] vaccine. Unresponsiveness to vaccination could be attributed to defect in a number of immunological regulatory mechanisms. In this study, IL-12 was quantitated in culture supernatant following in vitro stimulation of peripheral blood mononuclear cells isolated from a group of responder and non-responder neonates. Our results indicate significantly decreased production of HBsAg-induced IL-12 in non-responder subjects compared to responders [P<0.01]. Since IL-12 is produced mainly by antigen presenting cells [APC] and is considered to be crucial for initiation and polarization of CD4+ T-cell function, therefore, our findings could be interpreted to imply APC dysfunction in non-responder vaccines