Abstract
There are reports that fetal alcohol syndrome (FAS) is associated with immune deficiency or DiGeorge syndrome. To investigate the effect of prenatal alcohol exposure on the immune system, we used a mouse model of FAS in which C57BL/6J female mice were fed a complete liquid diet containing 25% ethanol‐derived calories (EDC) from gestational day (g.d.) 1 to 18. Thymus cell numbers were markedly reduced in 18‐day fetuses exposed to ethanol. Thymocytes from fetuses from the 25% EDC diet group and from pair‐fed and ad‐libitum control diet groups were compared by flow cytometry for expression of T cell differentiation antigens. The proportions of L3T4‐and Lyt‐2 positive thymus cells were significantly reduced in alcohol‐exposed fetuses compared to controls; however, the number of Thy‐1‐positive cells did not differ among any of the groups. Six‐day old neonates exposed prenatally to ethanol from g.d. 1 to 13 had thymus and spleen T cell populations similar to those of controls in almost all cases, indicating a “catch‐up” of T cell numbers in most animals. Spleen T cell function, assessed by response to Concanavalin A (Con A), or Con A plus T cell growth factors, was somewhat depressed in ethanol‐exposed 6‐day pups.