The fetal alcohol syndrome is associated with altered immunity. We attempted to delineate the mechanism of the decline in cell-mediated immunity observed by others by using rats which were exposed to alcohol in utero and tested for immune integrity 3 months after birth. We found that concanavalin A-stimulated T-lymphoblast (Con A T-blast) cells that were obtained from ethanol-exposed rats had significantly diminished proliferative responses to both crude and recombinant interleukin 2 compared to those obtained from normal and nutritional controls. The blunted response of Con A T-blast cells to interleukin 2 may be a biomarker of fetal exposure to alcohol.
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Norman et al. (1989) studied this question.