Immunology of pregnancy Flashcards

1
Q

What is pregnancy in terms of immunology?

A

‘Resetting’ of normal physiological state

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2
Q

What is the immunological paradox?

A

Fetus is 50% foreign material therefore there is a maternal investment to ensure that the genetic material is passed on

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3
Q

What happens at implantation?

A

Differential gene expression;

  • Increase in g.f. proteolytic enzymes and inflam mediators - FACILITATE IMPLANT
  • Change in exp of pt to prevent blasto rejection and inapp blasto invasion
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4
Q

What is the window of implantation?

A

Period where endometrium develops transient receptivity for embryo

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5
Q

What permits invasion of blasto?

A

Decidua

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6
Q

What is the primary decidual reaction

?

A

Uterine stromal cell enlargemnt

uNK prominent

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7
Q

How is intersitial invasion regulated?

A
  • Cytotb diff is faciliated
  • maternal decidua has permissive function
  • haemochorial placentation in humans
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8
Q

What can a cytoTB progenitor cell diff into?

A
  • CTB
  • EVT (invasive)
  • ScTB (fusion)
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9
Q

Why is the blasto not rejected>

A

It has modified self;non-self markers that do not trigger the immune system but instead tell the mother that it is safe and self

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10
Q

What are uNK cells?

A

NK cells that make up 70% of decidual immune cells
Exp Killer cell Ig-like R (KIR) which bind MHC-1 complex
Less cytotoxic that NK
Synth chemo/cyto that interact with EVT to facilitate invasion

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11
Q

What molecules are expressed on uNK cells?

A

CD56+ and CD16- (found on all other NK cells)

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12
Q

What HLAs do EVT express?

A

HLA-G, HLA-C and HLA-E

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13
Q

What is the role of HLA-G?

A

Only exp on TB - tells mother that it is self

Immunomodulation and preg-ass inflam

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14
Q

What is the role of HLA-C?

A

comb of HLA-C and KIR determines pregnancy outcome

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15
Q

What is the role of HLA-E?

A

Presents HLA-G leader peptide
inhib NK cell cytotox
Prevents EVT death

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16
Q

What signal does EVT present?

A

Says that TB cell is self and not dangerous - needed to stop TB degradation

17
Q

What combination of HLA and KIR promotes uNK cell activation and EVT invastion?

A

HLA-C1 and KIR2DS

18
Q

What happens if HLA-C2 and KIR2DL are present?

A

Poor EVT invasions
uNK cells are inhibited
Pre-eclampsia?

19
Q

What happens during interstitial invasion?

A

EVT migrate from cell columns
Invade decidual glands
Plug spiral artery - remodelling

20
Q

What drives endovascular invasion?

A

EVT and uNK

21
Q

When does endovasc invasion occur?

A

10-12 weeks

22
Q

What happens during normal endometrial invasion?

A

EVT invade artery to inner 1/3 of myometrium

23
Q

What happens if endo inv fails?

A

Inv localised to decidua and there is a decrease in maternal blood supply

  • preeclampsia
  • premature birth
  • FGR
  • RM
  • Placental abruption
24
Q

placenta creta

A

No decidua - invasion into myometrium and deeper
Poor placental separation
PP bleeding

25
Q

What happens to Th1:Th2 balance during pregnancy?

A

Th2 bias - prog inhib Th1 cell differentiation
Immune response is modified - more ab than cell-mediated
Fetus is protected

26
Q

What happens in abnormal pregnancy (Th1:Th2)

A

Th2 bias is not seen

Increased INFy and exagg inflam response

27
Q

Which ab crosses placenta?

A

IgG - enters fetal circulation and provides fetus with some immunity

28
Q

What happens to Ig that cross react with paternal HLA?

A

They are removed by macrophages

29
Q

Where are pat HLA foudn?

A

Placental macrophages and chorionic villus

30
Q

What is rhesus disease?

A

Where mother raises ab to fathers rhesus antigens. During first preg the mother creates the ab but they do not cross placenta
During second pregnancy there is rapid prod of IgG against R and they cross ScTb and lyse RBC - fetal anaemia

31
Q

How is rhesus treated?

A

With Anti-D which destroys Anti-R+ve IgG