Chronic prenatal stress contributes to poor birth outcomes for women and infants. Importantly, poor birth outcomes are most common among minority and low income women. To investigate underlying mechanisms, we tested the hypothesis that chronic stress related to minority or low income status is associated with glucocorticoid resistance as indicated by disruption in the cytokine-glucocorticoid feedback circuit. Home visits were conducted during which 3rd trimester pregnant women completed stress and depression surveys and provided blood for pro- and anti-inflammatory cytokines. Saliva was collected 5 times the preceding day for diurnal cortisol levels. For statistical analyses, women were grouped 3 ways, by race, income, and the presence or absence of either of those risk factors; this last group was labeled high or low general risk. Immune regulation was evaluated by evidence of a functioning negative feedback relationship between cytokines and cortisol. Of 96 participants, 18 were minority, 22 of low income, and 29 either minority or low income (high general risk). Pearson partial correlation identified a significant negative relationship between cortisol area under the curve (AUC) and pro- to anti-inflammatory cytokine ratios in the low general risk women (i.e., Caucasian, higher income) including IFNγ/IL10 (r=-0.73, p<0.0001), IL6/IL10 (r=-0.38, p=0.01), IL1β/IL10 (r=-0.44, p=0.004) and TNFα/IL10 (r=-0.41; p=0.005); no such correlations existed in the high general risk women (i.e., minority, low income) for (IFNγ/IL10: r=-0.25, p=0.43; IL6/IL10: r=0.12, p=0.70; IL1 β/IL10: r=0.05, p=0.87; TNFα/IL10: r=0.10; p=0.75), suggestive of glucocorticoid resistance. Cortisol levels throughout the day also were higher in minority and high general risk groups (p<0.05). Without cytokine glucocorticoid feedback, a pregnant woman's ability to regulate inflammation is limited, potentially contributing to adverse maternal and infant outcomes.