LECTURE 8

Question 1

What are innate defence mechanisms?

Answer 1

anatomic and physiological barriers (alternative complement pathway, phagocytes, NK cells, antimicrobial peptides)
rapid mechanism
early action as first line of defence

Question 2

What are acquired/adapted defence mechanisms?

Answer 2

antibodies, cell-mediated immunity
takes longer to develop but exhibits memory
enhances and focuses innate defences so less easily evaded by pathogens

Question 3

What is the action of CD4+ Th2 cells?

Answer 3

support antibody production, particularly class-switching to IgE
also activate eosinophils, basophils and mast cells

Question 4

What is the action of CD4+ Th1 cells?

Answer 4

activate macrophages and stimulate cytotoxic T cells (CD8)

Question 5

What are the three types of CD4+ T cells involved in responses?

Answer 5

Th1: active against intracellular pathogens
Th2: active against extracellular pathogens
Th17: active against extracellular bacteria and fungi, important in attracting inflammatory cells such as neutrophils

Question 6

What is the action of CD4+ Th17 cells?

Answer 6

attract inflammatory cells such as neutrophils
induced early in infection

Question 7

What are the two types of bacteria?

Answer 7

gram positive,
gram negative

Question 8

How do components of cell walls induce innate responses?

Answer 8

bind to toll-like receptors (TLR) on macrophages
10 TLR genes in humans: receptors recognise distinct molecular patterns on microbes (located on plasma membrane and endocytic vesicles)
NOD-like receptors (nucleotide binding oligomerisation domain - intracellular sensors - in cytoplasm)

Question 9

What are toll-like receptors?

Answer 9

Protein receptors within cell membrane of macrophages and dendritic cells

Question 10

What happens when PAMPs bind to TLRs?

Answer 10

Binding of pathogen-associated molecular patterns (PAMPs) to TLR can:
- promote inflammation
- promote dendritic cell maturation
- influence differentiation of T cells
- activate B cells (TI-1 antigens)

Question 11

How many human TLRs are there?

Answer 11

10

Question 12

How do bacteria protect themselves?

Answer 12

by having protective capsules

Question 13

What is effective against bacteria?

Answer 13

phagocytosis
can be opsonised by antibodies/complement

Question 14

Describe Streptococcus pneumoniae and how the vaccine for it works

Answer 14

Causes pneumonia, middle ear infection, meningitis
Antibodies to capsular polysaccharides protect against disease
Vaccine comprises 23 polysaccharide serotypes
Conjugate vaccine

Question 15

What is the role of antibodies in bacterial infections?

Answer 15

Opsonisation - binds Fc receptors on phagocytes
Complement Activation - promote inflammation via CEa, C5a, opsonise by binding C3b receptors on phagocytes, lysis of gram negative organisms (MAC,C5b,C6,C7,C8,C9)
Bind to and neutralise toxins
Bind to surface structures to prevent musocal adherence

Question 16

How is gram negative bacteria killed by complement lysis?

Answer 16

Defects in terminal complement components can lead to susceptibility to Neisseria spp.
MAC not most important component of complement, other defects have more widespread effects
Bacterial cell division vulnerable -> cell death

Question 17

Why are macrophages activated?

Answer 17

Th1 response drives macrophages to be more effective
Better at phagocytosis and killing
More efficient APCs
Stimulate inflammation (cytokines, prostaglandins)

Question 18

Give an example of an intracellular bacterium?

Answer 18

Mycobacterium leprae

Question 19

What is the difference between Tuberculoid and Lepromatous Leprosy and the response to each?

Answer 19

Tuberculoid: strong Th1 response, few live bacteria, slow progression, layers built around it for granuloma formation
Lepromatous: strong Th2 and antibody response (causes cell death), large number of bacteria in macrophages, disseminated infection, fatal