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  Indian J Med Microbiol
 

Figure 1: (a) Exposure of embryos to IFN-γ in culture is lethal, and it increased IFN-γ at the time of implantation. Mouse models implicate that IFN-γ response after malaria and toxoplasma infection mediates some of the placental defects and that IFN-γ overexpression leads to abnormal brain development in mouse models. (b) Type I IFNs (including IFNα and IFNβ) contributes to aberrant placental development after ZIK virus infection, as described in mouse models. (c) Exposure of embryos to TNF-α can induce an inhibition in development. TNF-α is a mediator of fetal demise in mouse models of immune stimulation (CpG, LPS, and Poly(I:C). TNF-α injection in mice can cause neural tube defects. Intraamniotic infusion of TNF-α is sufficient to induce preterm birth in non-human primate models. (d) IL-6 induces aberration in brain development and behavior in mouse models of maternal immune activation. (e) IL17 induces abnormal brain development and behavior in mouse models of maternal immune activation. (f) IL-1 may induce preterm birth, as amniotic IL-1β administration is sufficient to induce preterm labor in non-human primates. Mouse models reveal that IL-1 may mediate defects associated with peripartum intrauterine inflammation including abnormal lung development associated with bronchopulmonary dysplasia and brain injury

Figure 1: (a) Exposure of embryos to IFN-γ in culture is lethal, and it increased IFN-γ at the time of implantation. Mouse models implicate that IFN-γ response after malaria and toxoplasma infection mediates some of the placental defects and that IFN-γ overexpression leads to abnormal brain development in mouse models. (b) Type I IFNs (including IFNα and IFNβ) contributes to aberrant placental development after ZIK virus infection, as described in mouse models. (c) Exposure of embryos to TNF-α can induce an inhibition in development. TNF-α is a mediator of fetal demise in mouse models of immune stimulation (CpG, LPS, and Poly(I:C). TNF-α injection in mice can cause neural tube defects. Intraamniotic infusion of TNF-α is sufficient to induce preterm birth in non-human primate models. (d) IL-6  induces aberration in brain development and behavior in mouse models of maternal immune activation. (e) IL17 induces abnormal brain development and behavior in mouse models of maternal immune activation. (f) IL-1 may induce preterm birth, as amniotic IL-1β administration is sufficient to induce preterm labor in non-human primates. Mouse models reveal that IL-1 may mediate defects associated with peripartum intrauterine inflammation including abnormal lung development associated with bronchopulmonary dysplasia and brain injury