Block B

Question 1

Extracellular Pathogens

Answer 1

Bacteria
-Streptococcus pneumoniae
-Vibrio cholera
-Neisseria gonorrhoeae

Parasites
-worms

Question 2

Humoral Activation Phase

Answer 2

1. phagocytosis of pathogen by APCs
2. antigen processing/presentation
3. educate naive T cell
4. clonal expansion of T cell

Question 3

Humoral Effector Phase

Answer 3

1. uptake of pathogen by B cell
2. antigen processing/presentation
3. interaction with antigen-specific T cell
4. clonal expansion of B cell and Plasma cell differentiation

Question 4

IgA

Answer 4

-monomeric and dimeric forms
-dimeric survives on mucosal surfaces
-most IgA present in gut - 50mg/kg/day produced
-defense against intestinal pathogens (Rotavirus)
-in genital-urinary tract - protects against HIV (neutralise viral particles)

-selective IgA deficiency - most common Ab deficiency
-can appear asymptomatic (IgM can compensate)

Question 5

IgG

Answer 5

-secreted later in primary response
-main antibody class in secondary response
-gives long-term protection
-crosses placenta to provide neonatal protection until immune system develops
- >75% of total Ig in blood
- mediated in phagocytosis and opsonisation, Ab-dependent cellular cytotoxicity by NK cells, and degranulation of neutrophils, eosinophils and mast cells

Question 6

IgD

Answer 6

-inserted in B cell membrane, acts as BCR for antigen
-antigen-naive mature B cells express surface IgD and IgM in humans
-short half-life of ~3 days
-protective against mucosal pathogens (binds to Moraxella catarrhalis and Haemophilus influenzae
-IgD increases in serum of people with respiratory pathogens (rubella virus)

Question 7

IgM

Answer 7

-first Ab produced in primary response
-short half-life
-present in newborns - natural IgM
-produced in response to antigenic stimulation of B cells - adaptive IgM
-can recognise many microbial components
-high avidity of polymeric IgM - can immobilise target at a site

Question 8

IgE

Answer 8

-worm infestations, type 1 allergic reactions
-mediated via degranulation of granulocytes
-IgE-mediated activation through FcεRI on mast cells. Multivalent antigens cross-link receptor-bound IgE to trigger degranulation
-Pro-inflammatory response induces Th2 response
-protected against venom via IgE bound to mast cells

Question 9

Six Antibody Effector Functions

Answer 9

1. Neutralise
2. Agglutinate
3. Opsonisation
4. Activate complement cascade
5. Antibody-dependent cell-mediated toxicity (ADCC)
6. Trigger degranulation of granulocytes