Tutoring at home

Parturition, the bringing forth of young, encompasses all physiological processes involved in birthing: the prelude to (phase 0), the preparation for (phase 1), the process of (phase 2), and recovery from (phase 3) childbirth. From the disparate nature of these physiological processes, it is evident that multiple transformations in uterine function must be accommodated in a timely manner. Parturition can be arbitrarily divided into four uterine phases, which correspond to the major physiological transitions of the myometrium and cervix during pregnancy (Casey and MacDonald, 1993, 1997; Challis and associates, 2000). The phases of parturition should not be confused with the clinical stages of labor (first, second, and third stages), which comprise phase 2 of parturition.

Infections in utero have provided an opportunity to examine some of the mechanisms of the fetal immune response. Evidence of immunological competence has been reported as early as 13 weeks. Altshuler (1974) described infection of the placenta and fetus by cytomegalovirus with characteristic severe inflammatory cell proliferation as well as viral inclusions. Fetal synthesis of complement late in the first trimester has been demonstrated by Kohler (1973) and confirmed by Stabile and co-workers (1988). All components of complement are produced at an early stage of fetal development. In cord blood at or near term, the average level for most components is about half of the adult value (Adinolfi, 1977).
Fetal Immunocompetence
In the absence of a direct antigenic stimulus, such as infection, the immunoglobulins in the fetus consist almost totally of maternal immunoglobulin G (IgG) transferred across the placenta by receptor-mediated processes in syncytiotrophoblast. Therefore, antibodies in the fetus and the newborn infant are most often reflective of maternal immunological experiences.
Immunoglobulin G
Maternal IgG transport to the fetus begins at about 16 weeks and increases thereafter. The bulk of IgG is acquired during the last 4 weeks of pregnancy (Gitlin, 1971). Accordingly, preterm infants are endowed relatively poorly with maternal antibodies. Newborns begin to produce IgG, but slowly, and adult values are not attained until 3 years of age. In certain situations, the transfer of IgG antibodies from mother to fetus can be harmful rather than protective to the fetus. The classical example is hemolytic disease of the fetus and newborn resulting from D-antigen isoimmunization.
Immunoglobulin M
In the adult, production of immune globulin M (IgM) in response to an antigenic stimulus is superseded in 1 week or so predominantly by IgG production. In contrast, the IgM response is dominant in the fetus and remains so for weeks to months in the newborn. Because IgM is not transported from mother to fetus, any IgM in the fetus or newborn is that which it produced. Very little IgM is produced by normal, healthy fetuses, and that produced may include antibody to maternal T lymphocytes (Hayward, 1983). Increased levels of IgM are found in newborns with congenital infection such as rubella, cytomegalovirus, or toxoplasmosis. Serum IgM levels in umbilical cord blood and identification of specific antibodies may be useful in the diagnosis of intrauterine infection. Adult levels of IgM are normally attained by 9 months of age.
Immunoglobulin A
Differing from many animals, the human newborn does not acquire much in the way of passive immunity from the absorption of humoral antibodies ingested in colostrum. Nevertheless, immunoglobulin A (IgA) ingested in colostrum provides mucosal protection against enteric infections. This is likely also true for IgA ingested with amnionic fluid before delivery.
Lymphocytes
The immune system begins to mature early in fetal life. B lymphocytes appear in liver by 9 weeks and are present in blood and spleen by 12 weeks. T lymphocytes begin to leave the thymus at about 14 weeks (Hayward, 1983). Despite this, the newborn responds poorly to immunization, and especially poorly to bacterial capsular polysaccharides. This immature response may be due to either deficient response of newborn B cells to polyclonal activators, or lack of T cells that proliferate in response to specific stimuli (Hayward, 1983).
Monocytes
In the newborn, monocytes are able to process and present antigen when tested with maternal antigen-specific T cells.