Immune Functions in the Foetus and Infancy Flashcards Preview

HUMAN DEVELOPMENT > Immune Functions in the Foetus and Infancy > Flashcards

Flashcards in Immune Functions in the Foetus and Infancy Deck (26):
1

Which cells make up the innate immune system?

Granulocytes, natural killer cells, monocytes/macrophages and dendritic cells

2

Which cells make up the adaptive immune system?

T and B cells

3

Why is there so much variation in MHC/HLA receptors?

The genes which encode these receptors are both polygenic and polymorphic

4

How may the trophoblast play a role in preventing the rejection of a foetus?

The trophoblast doesn't present any classical HLA molecules so doesn't instigate T cell recognition. Presents the enzyme IDO which depletes tryptophan (required to activate T cells) so inhibits T cell activation. There is production of anti-inflammatory cytokines, which causes T regulatory cell development. Finally, they display HLA-G which engages inhibitory receptors on NK cells

5

From which stem cells does the immune system develop in the foetus?

Haematopoietic stem cells

6

Outline how the sites of haematopoiesis change throughout development of the foetus

1-3 months = yolk sac
1-7 months = foetal liver and spleen
4 months + = bone marrow

7

What is the immune system like at birth?

There is an abundance of naïve T and B cells in lymph nodes and spleen but few plasma or memory T cells due to little exposure to antigens in utero

8

When does T cell production begin in foetal development?

8 weeks gestation

9

Which maternal antibodies passively cross the placenta to the foetus?

IgG antibodies

10

Why is there a 'window of susceptibility' for an infant post-partum?

Antibody levels that were delivered via the placenta are now decaying, and there is a window where they have very minimal immune cells, making them susceptible to infection

11

How is maternal IgG transferred across the placenta to the foetus?

Via the neonatal FcR transporter

12

Name two problems that may occur due to the passage of IgG across the placenta

Haemolytic disease of the newborn or antibody mediated autoimmunity

13

Describe how placental IgG transfer may lead to haemolytic disease of the newborn

If the infant is RhD+ and the mother is RhD-, the IgG antibodies transferred to the infant will recognise them as foreign-antigens on the red blood cells, and therefore act to destroy the foetal blood cells, eliminating their circulatory system - this is generally only an issue in second pregnancy

14

How may issues with Rhesus factor discrepencies be treated?

Use of prophylaxis with antibodies to RhD (anti- D for example)

15

Describe how placental IgG transfer may lead to antibody-mediated autoimmunity, such as Graves' disease

Patient with Graves' makes anti-TSHR antibodies and these will be transferred across the placenta to the foetus, so the newborn infant with also have Graves', but ordinarily, the process of catabolism breaks down these maternal antibodies, and the newborn is cured

16

Why are more antibodies required in order to protect the body than harm, other than IgG, for example?

IgG gives systemic protection but doesn't protect mucosal surfaces

17

Where is IgA found in adults?

Lines mucosal surfaces (dimeric IgA) by being secreted onto the epithelia

18

Outline the function of IgA

Limits access of pathogens without risking inflammatory damage. It excludes and agglutinates pathogens but doesn't activate complement, recruit inflammatory cells or opsonise for phagocytosis

19

How is IgA secreted into breast milk?

B cells which recognise intestinal pathogens get activated in mother, then IgA-producing B plasma cells migrate to the breast and secrete IgA antibodies into the milk. On feeding the baby then passively acquires antibodies to the relevant pathogens

20

How may breastfeeding protect against allergies?

Exposure to antigens early on which leads to the appropriate development of T regulatory cells in the immune system

21

What are the characteristics of innate immunity in early life?

There are lower responses to PAMPs, reduced dendritic cell numbers and function, hypo-responsive NK cells and lower complement activity

22

What are the characteristics of adaptive immunity in early life?

There are poor antibody responses with poor responses to T cell help and reduced plasma cell survival

23

Why may the immaturity of the immune system in early life have consequences for vaccination programmes?

The supplied protective responses of vaccination may be poorly induced or short-lived due to the immaturity of the immune system as well as the potential interfering effects of maternal antibodies (e.g. masking of epitopes or negative signalling)

24

How may the development of the immune system in early life lead to the development of allergies?

If there is skewing of CD4 T cells responses to favour a Th2 response, this may favour asthma or allergy in some whereas an effective shift towards Th1 responses in early life may protect from allergy

25

Why is the newborn immune system immature at birth?

In the womb the foetus was required to co-exist with non-inherited maternal antigens, so a full immune system couldn't exist as rejection would have occurred. There may also be an argument that it is so that commensal microorganisms can help shape immune responses

26

Why is commensal gut microbiota beneficial?

It's required for normal development of the immune system, it aids in the digestion of complex carbohydrates and the microorganisms compete with pathogens