Humoural Immunity

Question 1

What are plasma cells?

Answer 1

B cells differentiate into plasma cells once stimulated by antigen:
• No longer circulate- settle in bone marrow or spleen
• Full of ER to produce antibodies
• Antibodies survive in blood for ~1 month but plasma cells likely survive longer

Change from producing cell membrane antibodies to soluble antibodies:
• Transcription starts at different point so exons coding for transmembrane region (M1 and M2) are missed out

—> enhanced secondary response to antigen as plasma cells producing correct antibody already exist

Question 2

What are the different antibody isotypes?

Answer 2

• IgG- γ heavy chain
• IgA- α
• IgM- μ
• IgD- δ
• IgE- ε

Light chain can be κ or λ (lambda)

Question 3

Outline antibody isotypes

Answer 3

• 5/6 different constant regions which can be used sequentially throughout course of B cell life, unlike V-D-J region which is permanent once differentiated
• IgG most common in blood
• IgA is specialised- secretory surfaces (gut, lung, mammary gland)- protection from organisms before entering the body but might not be that important- ~1/100 people deficient
• IgM found on naïve B cells and some in blood
• IgD found only on naïve B cells
• IgE mediates type I allergy/hypersensitivity- common allergies
• Isotype expresses depends on signals from innate immunity/Th cells
• IgA forms a dimer (4 Binding sites)- dimeric secretory IgA
• IgM forms a pentamer (10 sites)- pentameric circulating IgM

Question 4

What’s the effect of multivalency of Antibodies?

Answer 4

• Overall Binding strength measured by avidity not affinity which is much higher for multivalent antibodies
—> during primary response IgM is dominant antibody before correct IgG B cells have been selected
—> secondary response will be primarily IgG as it acts faster

Not all antibodies can be multivalent as it can cause large complexes which can settle in skin/kidney activating innate immunity and causing disease/pathology.

Some people can’t switch from IgM to IgG-> hyperinflammation diseases

Question 5

What are the effector functions of IgG and IgM?

Answer 5

IgG- neutralisation; toxins and viruses, direct opsonization and phagocytosis

IgM- complement activation

Question 6

Outline neutralisation

Answer 6

1. Toxins (Tetanus, Diptheria)
   • block binding sites of toxins then complex can be disposed of by macrophages in liver/kidney
   • in equilibrium- large amount of antibody needed
2. Viruses (some)
   • bind to binding sites on viral capsid (polio)
   • must be present before exposure- antibodies can not help once virus is inside cells

Question 7

How does opsonization impact phagocytosis?

Answer 7

• Encapsulated bacteria resistant to phagocytosis
• Antibody/Complement can coat bacterial capsule and then be recognised by phagocytic neutrophils
• Fc receptors allow phagocytes to bind antibody
• Binding to FcRλ (IgG) facilitates uptake and activates phagocytic killing mechanisms
• Vital importance- FcR deficiency results in high risk of bacterial infection

Question 8

What are monoclonal antibodies?

Answer 8

Derived from single clone of B cells
• Production of Antibodies of a single specificity:
• Immunised B cells fused to tumour cells-> keep dividing
• Specific B cell selected and cloned
—> Hybridoma technology

Question 9

Define humour all immunity

Answer 9

Immunity which exists in the cell-free part of blood, plasma or serum