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Infection and Immunity > L3 - Defence against infection > Flashcards

L3 - Defence against infection Flashcards

1
Q

Human pathogens can include…?

A

Parasites eg. worm, protozoan, fungi, viruses, bacteria.

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2
Q

The size of parasites which effect human varies between what parameters?

A

10nm (prions) - 10m (worms)

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3
Q

What are the two main extracellular sites of infection?

A

Interstitial spaces (+ blood and lymph) and epithelial surfaces.

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4
Q

What are the two main types of intracellular sites of infection?

A

Cytoplasmic eg. Listeria moncytogenes and vesicular eg. Tuberculosis causing bact.

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5
Q

To have an extracellular site of infection, bacteria must be have extracellular stages in their life cycle. This however, makes them susceptible to what kinds of host immunity mechanisms?

A

Antibodies, antimicrobial peptides, complement, phagocytosis, neutralization.

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6
Q

What kind of surface is IgA especially good at protecting?

A

Mucosal surfaces.

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7
Q

Which type of immune response uses pre-formed or rapidly formed components?

A

Innate immunity

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8
Q

What is the response time of innate immunity?

A

Minutes

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9
Q

What is the response time of adaptive immunity?

A

Several days

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10
Q

In which 3 ways does the adaptive response differ after repeated exposure?

A

Faster, stronger, qualitatively different ie. IgA response to repeated infection at mucosal surface or IgE response to Helminth worm.

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11
Q

In the adaptive response, each lymphocyte encodes a receptor to recognise A SINGLE/MULTIPLE antigen(s). Select the correct words.

A

A SINGLE antigen.

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12
Q

Clearing infections is the main role of which type of immunity?

A

Adaptive

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13
Q

Limiting local infection of tissues is the main role of which type of immunity?

A

Innate

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14
Q

3 main cell types of innate immunity and what kind of infections they fight.

A

NK cells (viral infections), Phagocytes ( bacterial and fungal infections), plasmacytoid dendritic cells (early anti-viral response).

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15
Q

Where is complement present in the body?

A

Anywhere, within interstitial fluid

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16
Q

What initiates the adaptive immunity?

A

Migrating dendritic cells

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17
Q

What are the 3 types of barriers which limit pathogen entry as a first line of defence?

A

Physical (+ mechanical), chemical, microbiological

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18
Q

Give examples of chemical barriers.

A

Fatty acids on skin (reduce change of bacteria colonising), low pH in stomach (reduces rate of bact. growth), enzymes like lysozymes in saliva and tears.

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19
Q

Examples of physical barriers

A

skin, nails, mechanical - flow of air and fluid across epithelia, movement of mucus by cilia

20
Q

Examples of microbiological barriers

A

normal flora compete for nutrients and attachment to epithelium, antibacterial substances produced like lactic acid, lactoferrin (chelates ferric ions, limiting microbial growth)

21
Q

What is the key complement component?

A

C3

22
Q

Explain the term ‘tickover activation’

A

C3 is slowly but spontaneously present in low conc. and cleaved in serum to produce C3a (soluble) and C3b

23
Q

How, why and to what does C3b bind?

A

C3b binds covalently to the bacterial cell membrane because it is unstable by itself.

24
Q

What are the 3 pathways of activation

A

Classical, alternative, mannose-binding lectin

25
Q

What does Factor B bind to and what happens when it does?

A

Factor B binds to C3b causing a conformational change (in Factor B) making Factor B susceptible to cleavage from Factor D. Ba is small and soluble so is released.

26
Q

Why does the rate of C3 cleavage rapidly increase during an infection?

A

During an infection the C3b (which has been generated by tickover activation) binds to a bacterial cell membrane. It then binds Factor B, which is cleaved by factor D (into Ba and Bb), leaving the C3bBb complex. This complex is a C3 convertase, so when bacteria is present, more of this complex forms, thus leading to cleavage of a lot of C3.

27
Q

What are the 3 outcomes of complement activation, regardless of the means of activation?

A

Recruitment of inflammatory cells, opsonisation of pathogens, killing of pathogens.

28
Q

What happens if another C3b associates with the C3bBb complex?

A

This creates (C3b)2Bb which is a larger complex with a different specificity. This complex is a C5 convertase and produces C5a (small and soluble) and C5b (remains bound to complex).

29
Q

Factors B and D are only involved in which complement activation pathway?

A

Alternative pathway.

30
Q

Mannose-binding lectin is a protein true or false?

A

True

31
Q

Bacteria cause macrophages to produce the cytokine IL-6, which in turn triggers hepatocytes to release what?

A

Acute phase proteins including mannose binding lectin.

32
Q

What does mannose binding lectin bind to?

A

Mannose residues on bacteria.

33
Q

What are the different specificities of MBL and ficolin?

A

MBL binds mannose and fructose residues and ficolins bind oligosaccharides containing acetylated sugars (on bacteria)

34
Q

What is the name of the enzyme family which contributes to complement activation?

A

MBL- associated serine proteases (MASP)

35
Q

When MBL binds sugar residues on bacteria and activates serine proteases, which complement components are cleaved?

A

C2 and C4.

36
Q

In the mannose binding lectin pathway which component binds covalently to the bacterial surface?

A

C4b.

37
Q

In the mannose binding lectin pathway, which complex acts as the C3 convertase?

A

C4bC2a

38
Q

In the mannose binding lectin pathway, which complex acts as the C5 convertase?

A

C4bC2aC3b

39
Q

The association of various components of the complement cascade has what effect?

A

Generating new specificity.

40
Q

What is the function of C3a and C5a?

A

Peptide mediators of inflammation, phagocyte recruitment

41
Q

What is the function of C3b?

A

Binds to complement receptors on phagocytes leading to opsonization of pathogens and removal of immune complexes

42
Q

What is the function of the terminal complement components (C5a, C6, C7, C8, C9)

A

Together they can form the membrane attack complex (MAC) which causes the lysis of certain pathogens and cells.

43
Q

Which component initiates the formation of the membrane attack complex and how?

A

C5b associates with C6 and C7. The C5b67 complex binds to the pathogen membrane via C7. Then, C8 is recruited to the complex and inserts into the cell membrane. C9 molecules bind to the complex and polymerise. Up to 16 molecules of C9 can come together to form a pore in the membrane.

44
Q

Staphlococci and Streptococci infections signal a defect in which member of complement activation?

A

C3 - as this is the key player for opsonisation of bacteria.

45
Q

Defects in the membrane attack complex (C5b-C9) are characterised by susceptibility to what types of infection?

A

Neisseria infections eg. Meningitis (Neisseria meningitidis and Gonorrhea (Neisseria gonorrhoea)

Infection and Immunity (28 decks)

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