The fetus can be compared to a haploidentical graft, sharing only half of the histocompatibility antigens of the “mother host”. As such, the fetus should be rejected by the immune system of the mother. At the same time, since the fetal immune system starts developing around the 9th week of gestation, the fetus should also mount a “graft-versus-host” reaction against those histocompatibility antigens that it has not inherited from the “mother host”. It follows that survival of the fetus – indeed of all mammalian species – is strictly dependent on a wide variety of mechanisms preventing graft rejection by the mother and graft-versus-host reaction by the fetus . Among the latter, a major role is certainly played by the slow intrauterine maturation of the fetal immune function, ultimately resulting in the physiological immune deficiency of the neonate that involves both innate and adaptive immunity. This immune immaturity – more severe in preterm and in very low birth weight infants - results in a weak immune response to antigen challenge and in the production of a poor immunological memory .
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