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Fetus > Immunology of pregnancy > Flashcards

Immunology of pregnancy Flashcards

1
Q

What are the maternal physiological adaptations to pregnancy

A

Endocrine, respiratory, cardiovascular, gastrointestinal, renal function + fluid homeostasis, reproductive, immune system, metabolic, resetting of normal physiological values

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2
Q

Why is pregnancy an immunological paradox

A

The fetus is 50% foreign
Maternal investment ensures genetic material is passed on
Maternal tolerance of fetal semi-allograft

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3
Q

Explain the differential gene expression at implantation

A

Increase in growth factors, proteolytic enzymes + inflammatory mediators to facilitate implantation
Change in expression of proteins involved in immune response to prevent blastocyst rejection and inappropriate blastocyst invasion
Very little of the immune system is fully downregulated as it is still required

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4
Q

Describe human implantation

A

Intestitial
Regulated invasive process
Hypoxic conditions (2-5% O2 relative to uterus)
Facilitates cytotrophoblast differentiation
Maternal decidua = permissive
Haemochorial placentation

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5
Q

What are 2 features of the primary decidual reaction

A

Uterine stromal cell enlargement

uNK cells more prominent

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6
Q

What is the function of cytotrophoblast cells

A

Fuse into multinucleate syncytiotrophoblast

Differentiate into invasive phenotype extravillous trophoblast cells responsible for differentiation

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7
Q

What is the function of uNK cells

A

Involved in synthesis of cytokines and chemokines

Facilitate EVT invasion

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8
Q

What are the steps of implantation

A
  1. Loose adherence/apposition
  2. Interstitial invasion
  3. Spiral artery remodelling and endovascular invasion
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9
Q

Describe interstitial invasion

A

EVTs migrate from cell columns
Invade decidual glands
Limited by decidua basalis
uNK cells may be required for or limit invasion

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10
Q

Describe spiral artery remodelling

A

Before- small bore, high resistance, facilitates hypoxia
EVTs plug spiral artery
Remodelled- wide bore, low resistance

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11
Q

Describe the immunological markers on maternal immune cells, EVTs, syncytiotrophoblast and uNK cells

A

Maternal immune cells- Normal self: non-self markers, normal immune response
EVTs- Modified self: non-self markers, modified maternal immune response
Syncytiotrophoblast- No self: non-self markers, MHC negative, no maternal response
uNK cells- CD56 +ve, CD16 -ve, KIR receptors

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12
Q

Describe the different HLAs and their functions

A

HLA-G: immunomodulation with IL8, IL10, VEGF, PGF. Involved in pregnancy associated inflammation
HLA-C: polymorphic, paternal specificity, combinations of HLA-C:KIR determine implantation outcome
HLA-E: presents HLA-G linear peptide, inhibits uNK cells cytotoxicity, prevents EVT death

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13
Q

What is an advantagous combination of HLA:KIR

A

Fetal HLA-C1 + maternal KIR-B (KIR2DS)

uNK cells activated, promotes EVT invasion

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14
Q

What is a disadvantagous combination of HLA:KIR

A

Fetal HLA-C2 + maternal KIR-A (KIR2DL)
uNK cells inhibited, poor EVT invasion
Pre-eclamspia

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15
Q

What are the observations that suggest T-helper cells function in pregnancy

A

Cell-mediated autoimmune disease (Th1) symptoms improve during pregnancy eg. rheumatoid arthiritis
Antibody-mediated autoimmune disease (Th2) symptoms worsen during pregnancy eg. systemic lupus erythematosus

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16
Q

What signals cause Th0 to differentiate into Th1

A

IL2, IL3, IL8, GM-CSF, INFy, high TNF

17
Q

What signals cause Th0 to differentiate into Th2

A

IL4, IL5, IL6, IL9, IL10, IL13, GM-CSF, low TNF

18
Q

What is the T-helper cell change during pregnancy

A

Placental fetal trophoblast cells secrete IL4 and IL10
Push Th0 towards Th2 differentiation
Th1 (cell mediated immunity) is modified/partly suppressed, humoral immunity still active

19
Q

What is the immunological basis of IUGR

A

Th2 bias not observed, INFy up, exaggerated inflammatory response, acute allograft rejection

20
Q

What is the normal maternal immune response to fetus

A

Maternal immune system removes antibodies that cross-react with fetal antigens- paternal HLAs presented on placental macrophages and chorionic villus.
Immune complexes removed by macrophages

21
Q

Why do maternal antibodies cross the placenta

A

Th2 cells promote B cell activation, antibodies made, IgG crosses the placenta and binds fetal Fc receptors on the syncytiotrophoblast, actively transported to chorionic villi, enters fetal circulation providing some immunity for fetus

22
Q

Describe Rhesus disease

A

Haemolytic disease of the newborn
Maternal IgG raised against paternal antigens on fetal red blood cells, cross reacting paternal antigens not removed
First pregnancy = sensitisation. Fetal blood mixes at term/postnatally, maternal immune response typically IgM but doesn’t cross placenta. Creates memory B cell.
Second pregnancy = rapid response. IgG due to memory B cells, cross the placenta. Lysis of fetal red blood cells causing fetal anaemia and fetal death

23
Q

What is Anti-D prophylaxis

A

In rhesus disease, Anti-D destroys the Rhesus negative IgG. Fetal red blood cells not attacked

24
Q

Describe normal and failed endovascular invasion

A

Normal- EVTs invade along artery into third myometrium, acquisition of maternal blood supply
Failes- invasion localised to decidua, reduced acquisition of maternal blood supply. Various pathologies- preeclampsia, prematurity, placental abruption, recurrent miscarriage, FGR

25
Q

What is an ectopic pregnancy

A

Pregnancy anywhere outside of the uterus. ~50% in ampulla, ~20% in isthmus. 22/1000 live birth.
More common with scar tissue
Absent/deficient decidua

26
Q

What is placenta creta

A

Absence of decidua
Affects 1/500-1000 pregnancies, more common with previous caesarean
Chorionic villi invasion
Low lying placenta
Requires uterine curettage
Risk of poor placental separation and significant postpartum bleeding
Acreta (75-80%) affects superficial myometrium
Increta (17%) affects deeper myometrium
Percreta (5%) penetrates uterine serosa, can affect other organs

Fetus (18 decks)

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