Two studies were conducted to assess the potential long-term effects of prenatal stress on the cytokine-related inflammatory response in juvenile rhesus monkeys. Subjects were derived from two different pregnancy conditions. Study 1 involved endocrine activation of the pregnant female by daily adrenocorticotropic hormone (ACTH) injection across a 2-week period (days 120–133 post-conception). Pregnant females in Study 2 experienced a psychological stressor, 10 minutes per day, for a 6-week period (days 106–147 post-conception). When the offspring from these pregnancies were 1.5–2 years of age, they were administered recombinant human interleukin-1β (rhIL-1β) to stimulate the release of endogenous cytokines, elicit fever, and activate the hypothalamic–pituitary–adrenal (HPA) axis. Cerebrospinal fluid (CSF) and blood levels of interleukin-6 (IL-6) were measured, as well as cortisol levels and body temperature. The prenatal ACTH treatment altered the postnatal response to IL-1β in juvenile offspring. These monkeys showed a significantly blunted response to the IL-1β, with smaller increments in blood and CSF levels of IL-6 and diminished temperature responses to the IL-1β. In contrast, the prenatal psychological stressor was not as potent and did not have lasting effects on this physiological response in juvenile monkeys. IL-1β also induced significant increases in cortisol secretion, but this adrenal response was comparable in all monkeys. These data suggest that differences in the prenatal environment could have a selective effect on cytokine physiology accounting for individual differences in the inflammatory response.