Perinatal depression is an emerging field with questions that remain to be answered, including the underlying pathogenesis, treatment and counseling. Pregnant women with depression represent a serious risk to themselves due to negative fetal/obstetrical and neonatal outcomes and to their child with respect to development later in life. The immune system plays a crucial role in major depression disorder (MDD), and studies indicate that both immune mediators (cytokines, chemokines) and neuroendocrine hormones cross-talk in MDD. However, the innate immune system is an unexplored field, and its link with prenatal depression has not been fully explored. The innate immune system is tightly regulated during early implantation and placentation of the conceptus, and such regulation is crucial for a successful pregnancy. T lymphocytes, which comprise helper T lymphocytes (Th), and cytotoxic T lymphocytes (CTLs), have been shown to be abundant at the fetal-maternal interface together with the recruitment of different subsets of immune cells [uterine Natural Killer cells (uNK), uterine Dendritic cells (uDCs), uterine Macrophages (uMΦs)] during decidualization of the endometrium. Pregnancy is considered to be an inflammatory process in which a Th2 over a Th1 immune response is critical for allowing the development the fetal allograft. Stressful stimuli and prenatal infections have been shown to deregulate the Th1/Th2 balance and are associated with increased production of proinflammatory cytokines and modification of neonatal immune responses via toll-like receptor (TLR) signaling. The innate immune system could represent a new frontier in exploring the etiology of several mental disorders, as suggested for schizophrenia. However, it is not clear how the innate immune system cross-talks with the fetal brain during perinatal depression.
Innate immune system, immune cells, depression, pregnancy, stress hormones.