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Medsci 314 > Lecture 19; Immunity in Reproduction > Flashcards

Lecture 19; Immunity in Reproduction Flashcards

1
Q

What are the three major branches of the immune system;

A

Physical barriers
Adaptive Immunity
Innate Immunity

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2
Q

When does the first barrier to infection (Skin) develop?

A

Outer layer of epithelium (Stratum Corneum) builds up to several layers during the third trimester

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3
Q

What do preterm babies (<30 weeks) have an increased risk for?

A

Preterm infants <30 weeks are at increased risk of infection due to underdeveloped skin

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4
Q

At what point does skin provide ‘adult’ protection?

A

2–3 weeks post partum skin provides “adult” protection regardless of gestational age

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5
Q

Describe the genesis of neutrophils in the fetus;

A
  • 6–8 wks Yolk sac

* 8–12 wks Liver & bone marrow

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6
Q

What happens to preterm babies neutrophil count?

A

• Low number of neutrophils found in mid
gestation fetuses & preterm infants
• Preterm neutrophils functionally deficient (e.g. migration, adherence)

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7
Q

What produces macrophages and monocytes in the fetus?

A

Monocytes & macrophages
• Yolk sac 1st trimester
• Bone marrow 2nd trimester

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8
Q

Despite producing adult numbers of macrophages and monocytes, what is wrong with these in the fetus?

A

• Fetus can produce “adult” numbers but function is reduced
– Reduced synthesis of cytokines (e.g. GM-CSF, IL-6) – Reduced response to GM-CSF
– Reduced migratory activity

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9
Q

In terms of leukocytes, what is one of the dominant cells in the fetus from early on?

A
  • One of the dominant fetal cell types in the placenta, especially in the 1st trimester
  • Function is unknown (potentially vasculature development)
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10
Q

When does complement synthesis in the fetus occur?

A

• Synthesised by fetus
– At term 50% of adult levels
– Adult levels reached by 6–18 months

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11
Q

Summerise the development of the innate immune system in the fetus;

A

• Components are produced in different tissues/locations during gestation
• Most components are present at birth (term)
• Most components have reduced
function/quantity
• Some components have non-immune roles

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12
Q

Where do fetal B cells develop?

A
  • 3 weeks Yolk sac
  • 8 weeks Liver
  • 12 weeks Bone marrow (30 weeks exclusive)
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13
Q

At 10 weeks the pre b cells that are produced, what are their functions?

A

– In mice become anergic upon exposure to antigen – Help to induce tolerance to self antigens?

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14
Q

Describe the b cell immunoglobulins produced over time in the fetus? I.e their receptors

A
  • week15–IgM
  • week20–IgG
  • week30–IgA

(class switching)

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15
Q

What are fetal b cells more susceptible to?

A

Tolerance

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16
Q

At what point are the adult levels of B cells?

A

22 weeks

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17
Q

At what point in time can a humans B cells isoswitch easily?

A

• Fetal/neonatal B cells differentiate to IgM secretory cells readily, but do not readily undergo class-switching to IgG or IgA secretion until 2 and 5 years respectively

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18
Q

At what point does the thymus develop?

A

• Thymus is formed by 8 weeks (rudimentary )

16 weeks is similar to term structure

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19
Q

Where do preT cells initially come from?

A

• Pre T cells migrate to thymus from yolk sac, liver & bone marrow from ~8 weeks

20
Q

At what point do we see adult levels of T cells?

A

• 16–20 weeks T cells and T cell subpopulations CD4+ & CD8+ at adult levels

21
Q

Are the genes of fetal APC similar to adult ones?

A

Gene expression mapping shows fetal and adult APS express similar genes

22
Q

What are the fetal DC genes?

A
  • DC1
  • (Conventional) cDC2
  • CD14+monocyte/macrophages
  • Fetal APCs in midgestation express tissue specific markers (eg lung cf gut)
23
Q

what is the inflammatory profile like in the fetus?

A

The fetus has a stronger anti-inflammatory profile than inflammatory

24
Q

At what point do DC start to circulate the lymphatics?

A

Gut and skin DCs migrate in lymphatics to lymph nodes from 16 weeks

25
Q

What point do T cells enter the lymph nodes?

A

• The lymph nodes contain T cells from 10 weeks

26
Q

When can the fetus mount a conventional T cell mediated response?

A

• Can mount a conventional T cell mediated

response from about 17 weeks gestation

27
Q

How do Fetal DCs differ in mixed lymphocyte reactions to adult DCs?

A

– Fetal DCs induce CD4+, CD25+, FOXP3+ CD127- CTLA4+ Tregs preferentially

– Fetal DCs stimulate CD8+ T cells less than adult DCs

28
Q

What point is the fetus capable of mounting an acquired immune response?

A

• 20 weeks the fetus has the capability to mount an acquired immune response
– i.e. B cells (IgG/IgM) and T cells (Tc/Th)

29
Q

At what point is the fetus capable of producing a term antibody production response?

A

Preterm infants >23 weeks can mount an immune response (antibody production) similar to a term neonate

30
Q

Is the uterus sterile?

A

No placental microbiome

31
Q

How can the fetus gain immunity?

A

• Fetus gains immunity by ACTIVE transport of IgG from maternal blood across the placenta

32
Q

What receptor is necessary for the active transport of IgA across the placenta?

A

• Requires a specific receptor

– FcyRn – consists of b2 microglobulin and an HLA-like a chain- binds IgG in acidic endosomes (pH 6.0)

33
Q

When does most maternal IgG transport occur?

A

• Most IgG transport occurs after 22 weeks

– Maternal levels reached at 34 weeks then exceeded

34
Q

When does the fetus begin to produce its own IgG?

A

• Following delivery (and exposure to antigen) the neonate begins production of Ig’s

35
Q

What is another source of aquired immune response?

A

Breast feeding

36
Q

What is in breast milk that makes it an aquired immune response;

A

– lgA major immunological factor in milk
– 5–7.5 mg/L slgA (more in colostrum)
– Breastfed infant up to 0.5 mg lgA/day
– Sterile gut of neonate rapidly colonised by various species e.g. E. coli, Klebsiella

37
Q

What is responsible for Haemolytic disease of the new born?

A

Maternal immune reaction to Rh antigens, particularly Rh D is responsible for HDN

• The Rh (rhesus) blood antigen system differs from the classical A, B, O groups

38
Q

What is haemolytic disease of the new born?

A
  • Mum Rh- & dad Rh+ then babe will be Rh+
  • Fetal blood into maternal circulation
  • Sensitisation of maternal immune system & anti-Rh antibodies
  • In subsequent pregnancies antibodies cross placenta & destroy fetal RBCs (not a problem in first pregnancy)
39
Q

How can haemolytic disease of the newborn be tested for?

A

1) Direct Test (AB there)

2) Indirect test (AB added)

40
Q

What are the treatments for HDN?

A

Anti D Prophylaxis

Interuterine Transfusion

Intravenous Immunoglobulin

41
Q

What happens in anti D prophylaxis?

A

– Antibodies to Rh D antigen produced in volunteers by RBC immunisation
– γ globulin fraction purified & administered to Rh- mothers of Rh+ babies following delivery
– Passive immunisation destroys transfused fetal RBCs before a strong maternal response

42
Q

What happens in interuterine transfusion?

A

– Used for Rh-ve women who already produce antibodies to Rh antigens (due to previous Rh +ve pregnancy)
– A fetus effected by HDN is transfused in utero with maternal-compatible blood injected into an umbilical vessel or the abdominal cavity
– Initially done using x-ray guidance now much improved by use of ultrasound

43
Q

What happens in intravenous immunoglobulin?

A

– Alternative to intrauterine transfusion
– Mechanism not clear
• Possibly occupying Fc receptor sites, thus competing with the anti-D sensitised neonatal erythrocytes & preventing further haemolysis

44
Q

How does the placenta protect from autoantibodies?

A
  1. IgM/IgA autoantibodies do not enter the fetal circulation e.g. rheumatoid factors, ANA
  2. Organ “non-specific” antibodies may encounter their antigen and be trapped in the placenta - the placental “sink”
45
Q

Do all autoantibodies not cross the placenta?

A

• Many autoantibodies do cross the placenta
– Cause symptoms in fetus
• Myasthenia gravis: acetyl choline receptor antibody
• Thyrotoxicosis: antibody stimulates thyroid

• These autoantibodies induce transient disease which resolves upon catabolism of the maternal antibody

46
Q

What autoantibodies can cause still birth?

A
  • Fetal death (still birth/miscarriage)
  • Exact mechanisms unknown but appear to attach the placental trophoblast
  • Rapidly enter the syncytiotrophoblast via receptor (not FcRn) mediated process and disrupt mitochondrial function

Medsci 314 (31 decks)

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