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CMB2004 > L9 - Immunity against infection > Flashcards

L9 - Immunity against infection Flashcards

1
Q

Organisms that may cause disease

A
  • Bacteria
  • Viruses
  • Fungi
  • Parasites

Pathogens have evolved ways of escaping host defense mechanisms

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2
Q

Different effector mechanisms needed, dependent on:

A
  • Type of pathogen
  • Localisation
  • Challenge
  • Stage of infection
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3
Q

Host defence mechanisms

A

Innate defence mechanism

Specific/adaptive defence mechanism

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4
Q

Innate defence mechanism

A
  • Rapid
  • Barriers, complement (alternative pathway), phagocytes, NK cells
  • Act early: first line of defence
  • Non-specific
  • Ineffective against many pathogens
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5
Q

Specific/adaptive defence mechanism

A
  • Antibodies & cell mediated immunity
  • Takes longer to develop
  • Exhibit memory
  • Enhances & focuses innate defences
  • Less easily evaded by pathogens
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6
Q

What are the types of T helper cells (CD4+)?

A

TH1
TH2
TH17

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7
Q

TH1 CD4+

A

Active against intracellular pathogens

Activate macrophages and stimulate cytotoxic T cells (CD8+ cell)

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8
Q

TH2 CD4+

A

Active against extracellular pathogens

Support antibody production, particularly class-switching to IgE

Also activate eosinophils, basophils and mast cells

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9
Q

TH17 CD4+

A

Active against extracellular bacteria and fungi, important in attracting inflammatory cells such as neutrophils

Induced early in infection

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10
Q

Difference between gram positive & gram negative bacteria

A

Thick layer of peptidoglycan in gram positive cell wall

Gram negatives have an outer membrane containing LPS

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11
Q

How do bacteria induce innate responses?

A

Components of cell walls (eg. LPS, peptidoglycan) can induce innate responses

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 oligomerization domain (intracellular sensors)

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12
Q

What are PAMPs?

A

Pathogen-associated molecular patterns

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13
Q

What happens when PAMPs bind to TLRs?

A
  • Produce inflammation
  • Promote dendritic cell maturation
  • Influence differentiation of T cells
  • Activate B cells (TI-1 antigens)
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14
Q

Cellular location of TLR

A

TLRs in the endosome membrane recognise microbial components that are only exposed after the microbe has been broken down

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15
Q

Phagocytosis often effective against bacteria

A

Bacteria may have protective capsules

Can be opsonised by antibody/complement

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16
Q

Role of antibodies in bacterial infection

A

Opsonisation

Complement activation

Bind to & neutralise toxins

Bind to surface structures to prevent mucosal adherence

17
Q

Opsonisation by antibodies

A

Bind Fc receptors on phagocytes

18
Q

Complement activation by antibodies

A

Promote inflammation via C3a, C5a

Opsonise by binding C3b receptors on phagocytes

Lysis of Gram negative organisms (MAC C5b,C6,C7,C8,C9)

19
Q

How can gram negative bacteria be killed?

A

By complement lysis

20
Q

How do some bacteria survive within phagocytes?

A

Inhibit lysosome/phagosome fusion

e.g. Mycobacterium tuberculosis

21
Q

Activated macrophages do what?

A
  • Better at phagocytosis and killing
  • More efficient antigen presenting cells
  • Stimulate inflammation (cytokines, prostaglandins)
  • Macrophages are central to a TH1 response
22
Q

Example of intracellular bacterium: Mycobacterium leprae

A

Outcome depends on the type of response

Tuberculoid leprosy: strong TH1 response, few live bacteria, slow progression, granuloma formation

Lepromatous leprosy: strong TH2 and antibody response, large no. of bacteria in macrophages, disseminated infection, fatal

23
Q

Protection against bacterial infection

A

Antibodies important in protecting against extracellular pathogens

T cell effector mechanisms protect against intracellular organisms

CMB2004 (12 decks)

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