PRENATAL ALCOHOL EXPOSURE SELECTIVELY SUPPRESSES CELL-MEDIATED BUT NOT HUMORAL IMMUNE RESPONSIVENESS

The present study examined effects of fetal alcohol exposure (FAE) on the ability of peripubertal male and female rats to mount a humoral immune response against T-cell-dependent as well as independent antigens. The appropriate pair-fed (PF) and control (C) cohort rats were included. Serum immunoglobulins (Ig) levels were determined following a primary or secondary immune response. In addition, plasma corticosterone levels were measured in conscious, freely moving FAE, PF and C rats following sensitization with the T-cell-dependent antigen sheep red blood cells (SRBC). The study demonstrates that, in response to primary or secondary immunization, serum Ig levels in FAE rats were not significantly different from those in the PF or C cohorts. On the other hand, a marked reduction in mitogen-induced T-cell proliferative response was observed in FAE male rats in the same age group. Plasma corticosterone concentrations were increased almost four-fold 7 days after the primary immunization with SRBC, but there were no significant differences among the FAE, PF or C groups. Taken together, evidence from in vivo and in vitro studies indicates that FAE is associated with a selective impairment of cell-mediated immune function, including mitogen-induced T-cell proliferation, graft versus host as well as contact sensitization responses, but not of humoral immune function.