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Reproductive Biology > Immunology and Pregnancy > Flashcards

Immunology and Pregnancy Flashcards

1
Q

Why is the immune system relevant?

A

The fetus is an allograft - is not 100% made of mums DNA and should be rejected like a foreign graft

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2
Q

What are the arms of the immune system?

A

Innate (recognise danger) and adaptive (recognised non-self)

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3
Q

3 sections - what do they recognise, negative selection, antibody?

What do B cells do?

A

They recognise soluble antigen and produce antibodies that have antigen specific receptors (BcR).

During development antigen specific receptors that bind to self antigens are killed in negative selection

The antibody is a soluble version of the BCR and bind to pathogens and targets them for killing

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4
Q

What is a T cell receptor and what does it bind?

A

This is analogous to antigen binding region of an antibody/BcR but can’t bind to soluble antigen directly. Antigen peptides must be presented on MHC.

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5
Q

What is negative selection and positive selection in T cells development?|

A

Negative selection - any that bind to self antigens are killed (some become Tregs to give autoimmunity)

Positive selection - T cells that won’t bind to self MHC are killed

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6
Q

What do class 1MHC present and to what cell?

A

intracellular antigens to cytotoxic T lymphocytes (CTL)

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7
Q

What do class 2 MHC present and to what cell?

A

extracellular antigens to helper T cells

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8
Q

What is MHC class 1 found on?

A

All nucleated cells

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9
Q

How does class 2 MHC show antigen to T cells?

A

The alpha and beta chains of the MHC form a tetramer with invariant chain and then they go into the endosome where they are cut by proteases before being shown to CD4 helper T cells

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10
Q

What are the T helper cells?

A

Th1 TH2 Th17 and Tregs and what they differentiate into depends on singals from the innate immune system

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11
Q

What do TH1 cells do?

A

These recruit macrophages, are inflammatory but can cause tissue damage/autoimmunity

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12
Q

What can Th2 cells do?

A

Kill parasites and cause allergies

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13
Q

What do tregs do?

A

Supress other immune responses and supresses autoimmunity

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14
Q

What are CTL’s?

A

Induces apoptosis through perforin/granzymes

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15
Q

How do T cells respond to allografts?

A

They kill them

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16
Q

Why do NK cells kill and not kill cells?

A

Primed to kill any cell unless told not to by KIR binding on MHC on surface of the cell and preventing killing

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17
Q

what is the placental membrane and what does this mean?

This is the name of the type of placental membrane not like describing

A

A syncytium which means no cell junctions for maternal immune cells to migrate between and no lymphactics

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18
Q

Does fetal tissue express any MHC 2 or MHC1 and why?

A

express no MHC2 and some MHC1 (mainly HLA-C) which causes them to escape the CTL response

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19
Q

What happens to the NK cells as these should attack the lack of MHC?

A

Fetal tissue expresses HLA-E and HLA-G which bind to the NK cell inhibitory receptors and they have a specialised phenotype

20
Q

What is the decidua dendritic cell and what do they produce?

A

APC’s that are very rare in the decidua which might not be able to exit into the lymph node. They produce IDO and a tolerised phenotype induing a TH2 response.

21
Q

What are decidua macrophages?

A

Type of phagocyte which can be inflammatory, kill invaders etc (M2) or anti-inflammatory (M1)

22
Q

what type of macrophages are peri implantation macrophages?

A

M1

23
Q

Later in development they become M2 macrophages - what do these express?

A

IDO and IL-10 (both immunosuppressive)
Have roles in reorganisation of vasculature in early pregnancy

24
Q

How is the fetus protected by apoptosing fetal specific T cells?

The pathways of 2 ligands

A

FasL binds to Fas on activated T cells killing them.
OR
Gal-1 is expressed by decidua NKs, macrophages and endometrium which induces apoptosis of T helper cells and supresses DC.

25
Q

What does IDO expressed by decidua and trophoblasts do?

A

Catabolise tryptophan to metabolites such as kynurenine and picolinic acid (these inhibit T cell and NK cell activation).

26
Q

What can Kyrunine also do (made by IDO)?

A

Apoptosis of Th1 not Th2 cells

27
Q

What does chemically inhibiting IDO lead to?

A

Rejection of allogeneic but not syngeneic fetuses

28
Q

What does a reduction in Tregs do in pregnancy?

A

They cause spontaneous abortion if joined with increased inflammatory T helper cells

Pre-eclampsia with increased blood inflammatory: regulatory T cell ratio

29
Q

What happens if you deplete the Tregs in early pregnancy?

A

No effect of depletion in syngeneic pregnancy
Reduced viable offspring in a allogeneic mice

30
Q

CNS1-KO mice can’t make what?

A

New Tregs

31
Q

What are Tregs induced by?

A

TGF-beta, Gal-1 and IDO

32
Q

What does phosphocholine do in pregnancy?

A

supresses T and B cell proliferation and inflammatory responses in RA

33
Q

What is the complement system?

A

activation results in cascade of cleavage, activation and inflammation which results in the formation of the membrane attack complex to put lysis pores in cells

34
Q

What does Crry the complement protein do?

A

Prevents deposition of C3 and C4 and knocking this out leads to unsuccessful births

35
Q

What are bystander immune supression things?

A

Reduced allergy, RA, MS but increased susceptability to infection e.g. malaria, HIV and listeria

36
Q

Can the inflammatory immune response to bacterial infectons lead to preterm labour?

A

Yes

37
Q

What causes HDN?

A

Maternal antibody responds to paternal antibody on the fetal red blood cells causing anaemia, jaundice, brain damage and even death

38
Q

How do the HDN symptoms arise?

A

Lysed red blood cells release haemoglobin which is broken down into bilirubin turning skin yellow and entering brain to have toxic results

39
Q

What is passive immunity and how does this work?

A

Maternal antibodies can pass through the placenta using the neonatal antibody FcRn and maternal IgA is given to babies through breast milk. Allows baby to have a bit of an immune system

40
Q

What are the blood group antigens?

A

A,B and O and Rh

41
Q

What happens in Rhesus disease during the first pregnancy?

A

Mother Rh- and father Rh+ the first pregnancy is fine as the mother immune system has never seen this before and during delivary the fetal blood is given to the mother causing an anti-Rh antibody to be raised.

42
Q

Rhesus disease during the second pregnancy?

A

The anti-Rh antibodies can enter the fetus causing haemolysis of red blood cells. This gets worse with subsequent pregnancies.

43
Q

How is HDN treated - preventative?

A

Parents screened and if father Rh- and mother Rh+ the baby can be screened as can the mother again for antibodies.

44
Q

Treatment for HDN - if fetus is Rh+?

A

If fetus Rh+ then rhogam shot is given during pregnancy and after birth which binds the Rh antigen and prevents mother immune system from being sensitised

45
Q

Mild, Moderate, Severe

What happens if baby is affected by HDN?

Treatment

A

Mildly Affected - UV treatment (breaks down bilirubin)

Moderately Affected - blood transfusion to stop anaemia

Severely affected - Rh negative blood transfusion given every 10 - 21 days of gestation and treatment after birth

Reproductive Biology (21 decks)

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