Studies of maternal infection provide some evidence that modulation of immune response 28 and adverse effects on in utero maturation of critical brain structural and functional componenets 24 may correlate with increased risk of schizophrenia in offspring. From animal models, maternal infection can alter interleukin 6, interleukin 1b, or tumor necrosis factor a (TNF-a) in amniotic fluid or placenta and TNF-a in the fetal brain. 29 There is evidence that cytokines have an important function in the development of fetal neurons and glial cells, and abnormal levels of these (proinflammatory) cytokines may contribute to abnormal brain development, [30] [31] [32] [33] [34] at least in animals.