Causes: Immaturity & Pregnancy – Secondary Immunodeficiency Diseases

by Peter Delves, PhD

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    00:01 When we are very young, our immune system is not fully developed.

    00:05 So immaturity can also be a cause of secondary immunodeficiency.

    00:10 Neonates have a relatively immature immune system, particularly if delivered pre-term.

    00:15 There is susceptibility to infection and this correlates with the degree of prematurity.

    00:22 Both T-cells and B-cells in the neonate are naïve, they haven’t encountered antigen yet.

    00:29 And therefore they respond relatively slowly to infection.

    00:35 In some infants there is a transient hypogammaglobulinemia of infancy in which IgG levels remain low following catabolism of placentally-transferred maternal IgG.

    00:49 This is usually asymptomatic.

    00:52 Maternal IgG is transported across the placenta by the neonatal IgG-Fc receptor (FcRn).

    01:03 So antibodies from the mother are picked up by FcRn and transferred across the placenta, and released into the fetal circulation.

    01:15 The newborn therefore contains the same antibody specificities as the mother because the antibody is coming from the mother rather than being produced by the fetus.

    01:24 In immaturity, maternal IgA and IgG in breast milk is particularly important for the newborn.

    01:33 Ingested secretory IgA protects the newborn against microbial colonization in the gut.

    01:40 Whilst ingested IgG antibodies are transported into the infant’s circulation by the FcRn on gut epithelium.

    01:50 Here we can see the serum immunoglobulin levels in the newborn as a percent of adult values.

    01:59 Our own B-cells are beginning to make IgM antibodies before we’re born, but only very small levels are produced by the time of birth.

    02:10 But within the months following birth, IgM levels within a year or so reach the level that you would find in the adult.

    02:20 IgG follows a little bit later on, remember IgM is characteristic of the primary immune response and IgG of the secondary immune response.

    02:29 And at the time of birth, there is very little IgG in the infant’s circulation that is being produced by the infant’s own B-lymphocytes.

    02:38 They’re just reaching the stage of maturity when they can begin to make antibody.

    02:44 IgA levels are also vanishingly small at the time of birth but will increase over time.

    02:54 However, with respect to IgG, there is in fact quite a lot of IgG in the fetal circulation and in the newborn circulation.

    03:05 And that’s because IgG is transferred across the placenta as we’ve just seen using the FcRn.

    03:15 This maternally derived antibody will begin to be catabolised once the newborn has been born.

    03:23 And IgG has a half life of around about three weeks.

    03:29 So three weeks after birth, half of the maternal antibody will have been catabolised.

    03:35 Six weeks after birth, there’ll only be 25% of the maternal antibody.

    03:39 But the infant is now beginning to make their own IgG, so there will be a dip in the level as the maternal IgG is catabolised, but then the infant’s own IgG will come up and eventually there will be a rise in the overall IgG level.

    04:00 Pregnancy is a condition in which there is a natural immunosuppression.

    04:06 This occurs in order to avoid rejection of the semi-allogeneic fetus.

    04:11 Remember, half of the genes in the fetus, will have come from the male partner.

    04:19 Immunosuppression is largely focused at the maternal-fetal interface in the placenta, to stop an immunological rejection of this semi-allogeneic fetus where half of the genes are from the dad.

    04:33 However, there is some degree of systemic suppression of the immune response.

    04:38 And pregnant women have a degree of increased incidence and severity of infection.

    04:46 There is no evidence of risk of vaccinating pregnant women with inactivated virus or bacterial vaccines or with toxoids, which are inactivated bacterial toxins.

    04:57 However, live virus vaccines are contraindicated because of the theoretical risk of transmission of live virus to the fetus.

    About the Lecture

    The lecture Causes: Immaturity & Pregnancy – Secondary Immunodeficiency Diseases by Peter Delves, PhD is from the course Immunodeficiency and Immune Deficiency Diseases. It contains the following chapters:

    • Immaturity
    • Pregnancy

    Included Quiz Questions

    1. FcRn
    2. FcγRI
    3. FcγRIIb
    4. Poly Ig receptor
    5. FcεRI
    1. Placentally transferred maternal IgG is metabolized while the neonate produces their own IgG.
    2. T cells and B cells are naive and slow to react antigens.
    3. Immature immune system due to pre-term birth.
    4. Lack of innate immunity.
    5. Maternal IgG is replaced by IgM.
    1. 1 year old
    2. 28 days old
    3. 10 years old
    4. 6 months old
    5. 3 years old
    1. The mother must be immunosuppressed because developing fetus is semi-allogeneic.
    2. The mother must be immunosuppressed so that IgG crossing the placenta and being transferred to the fetus does not cause embryologic abnormalities.
    3. The mother must be immunosuppressed because the placenta is partially fetal tissue.
    4. The mother must be immunosuppressed so that the immune system does not turn against the fetus after being exposed to an endogenous antigen.
    5. The mother must be immunosuppressed in order to divert metabolic resources to the developing fetus.

    Author of lecture Causes: Immaturity & Pregnancy – Secondary Immunodeficiency Diseases

     Peter Delves, PhD

    Peter Delves, PhD

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