Role of Cytokines on Fetal Immune Programming

Fetal Immune Programming (FIP) is the reset of the normal fetal development due to the changes in the metabolic environment during critical period in the intrauterine life. Barker’s hypothesis states that, uterus is the first environment which the developing fetal immune system encounters. Several reports revealed that intrauterine growth retardation is the cause for increased risk of several non-communicable diseases to the fetus. FIP is connected with maternal immune milieu and hence has a significant impact on the fetal immune system. T-lymphocytes (T-cells) are important for coordinating the immune response and can be characterized into subsets according to their phenotypic characteristics as type-1, type-2 and regulatory T-cells. Each T-cell subset has an exclusive functional role, including their capacity to produce proand anti-inflammatory cytokines in response to an immune challenge. Type 1 T cells produce, interferon-γ, interleukin-2 and tumour necrosis factor-α, which promote cellular immune responses, whereas type 2 T cells produce IL-4, IL-5, IL-9, IL10 and IL-13 that provide optimal help for humoral immune responses. Although it is known that T cell cytokines produced in response to fetal molecules could have a role in fetal programming and fetal immune outcomes, the molecular mechanisms underlying the regulation of the immune components at various levels are yet to be elucidated. The present review outlines the role of cytokines on fetal immune programming which would aid in understanding alarmingly increasing incidence of diseases associated with immune dysregulation in the fetus.