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BM 212: Introduction to Immunology > Block D Lecture 2: Immunity to Pathogens > Flashcards

Block D Lecture 2: Immunity to Pathogens Flashcards

1
Q

What is a parasite?

A

An organism which benefits at the expense of another organism (usually of a different species) called a host with the host not benefitting from the association
(Slide 3)

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2
Q

What is one way a host-parasite association may occur?

A

Due to the host being injured
(Slide 3)

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3
Q

What are 2 examples of unicellular parasites?

A

Leishmania
Toxoplasma
(Slide 3)

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4
Q

What is leishmaniasis caused by?

A

Protozoa (unicellular) parasites from over 20 leishmania species
(Slide 4)

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5
Q

What is known to transmit leishmaniasis?

A

Over 90 species of sandfly
(Slide 4)

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6
Q

What are the 3 main forms of leishmaniasis?

A

Visceral
Cutaneous
Mucocutaneous
(Slide 4)

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7
Q

What is the fatality rate in untreated cases of visceral leishmaniasis?

A

> 95%
(Slide 4)

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8
Q

What is the most common form of leishmaniasis?

A

Cutaneous
(Slide 4)

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9
Q

What 2 things does cutaneous leishmaniasis cause?

A

Skin lesions and ulcers
(Slide 4)

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10
Q

What is mucocutaneous leishmaniasis?

A

Partial or total destruction of mucous membranes of the nose, mouth and throat
(Slide 4)

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11
Q

What is crucial in healing cutaneous leishmaniasis?

A

Cell-mediated immune responses
(Slide 5)

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12
Q

What happens in healing cutaneous leishmaniasis?

A

Macrophages and dendritic cells produce IL-12 to activate macrophages to kill the parasite
Interferon-gamma from NK cells and Th1 also activate macrophages
The activated macrophages then produce microbicidal (agent that kills microbes) products
(Slide 5)

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13
Q

What happens in Non-healing cutaneous leishmaniasis?

A

Macrophages are not activated
IL-4 drives a Th2 response instead
Th2 produce IL-4 / IL-13 which inhibit a Th1 response by inhibiting IL-12 production or expression of IL-12Rß2 expression and they also inhibit IFN-gamma production and activity
(Slide 7)

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14
Q

What 2 things are important in healing toxoplamosus?

A

Cell-mediated immune response and humoral response
(Slide 9)

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15
Q

What is toxoplasmosis caused by?

A

Toxoplasma parasite
(Slide 9)

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16
Q

What cells can the toxoplasma parasite live in?

A

Any cell
(Slide 9)

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17
Q

What are the main mediators of toxoplasmosis?

A

Cytotoxic (CD8+) T cells producing IFN-gamma
(Slide 9)

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18
Q

What role does IgA play in protecting against toxoplasmosis?

A

Protecting gut mucosa
(Slide 9)

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19
Q

What happens to toxoplasma parasites coated in IgG?

A

They are killed inside macrophages following phagolysosome fusion
(Slide 9)

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20
Q

What 2 things must the body increase in order to expel gut nematodes?

A

Increased mucous production
Increased peristalsis (contraction and relaxation of muscles in the gastrointestinal tract)
(Slide 10)

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21
Q

What response does the body use to expel gut nematodes?

A

A cell-mediated Th2-dependent response
(Slide 10)

22
Q

What needs to infect host cells in order for a virus to replicate?

A

An “obligate parasite”
(Slide 12)

23
Q

What does an “obligate parasite” infecting host cells to replicate cause?

A

Damage to host cells known as “cytopathic effects”
(Slide 12)

24
Q

How does a virus often stop the infected host cell from completing its function?

A

As it hijacks the host cells machinery to make more viruses
(Slide 12)

25
Q

Why does a virus often kill the host cell?

A

As it ruptures to release new virus particles or virions
(Slide 12)

26
Q

What 3 things must an immune response against a virus do?

A

Kill virus particles - known as virions
Clear virus infected cells
Neutralise viral toxins
(Slide 12)

27
Q

What 3 things make up the innate response against viruses?

A

Type-1 interferon (IFN)
Natural Killer (NK) cells
Dendritic cells
(Slide 13)

28
Q

What 2 things make up the adaptive immune response to a virus?

A

T cells (both CD4+ and CD8+)
B cells
(Slide 13)

29
Q

What are the 2 different types of Type-1 Interferons?

A

IFN-α and IFN-ß
(Slide 14)

30
Q

What does cytokine production in a virus infected cell induce?

A

The cell to shutdown some of its protein-making functions and increase its RNA-cutting enzymes
(Slide 14)

31
Q

What are 2 ways some viruses try to evade immune response?

A

By switching off MHC-1 expression or inhibiting the processing pathway
(Slide 15)

32
Q

How much does IFN-α increase the activity of natural killer cells?

A

20-100 fold
(Slide 15)

33
Q

What do activated natural killer cells produce?

A

IFN-gamma
(Slide 15)

34
Q

What induces T cells towards the Th1 phenotype?

A

IFN-gamma
(Slide 15)

35
Q

What type of cytotoxicity do natural killer cells carry out?

A

Antibody-dependent cell-mediated cytotoxicity
(Slide 15)

36
Q

How are natural killer cells activated by altered self cells?

A

Altered surface proteins on infected cell might suggest infection resulting in a direct killing by an NK cell by inducing apoptosis (such as reduces levels of MHC-I)
(Slide 16)

37
Q

What do cytotoxic T cells produce on activation?

A

Granules
(Slide 18)

38
Q

How do cytotoxic T lymphocytes recognise infected cells?

A

It recognises the viral peptide-MHC class I receptor complex with it’s TCR
(Slide 18)

39
Q

What is MHC-1 expression increased by?

A

IFN-α
(Slide 18)

40
Q

What triggers cytotoxic T cell killing?

A

Recognition of specific viral antigen on MHC-I
(Slide 19)

41
Q

What do the intracellular granules activated by cytotoxic T cells activate?

A

Apoptosis
(Slide 19)

42
Q

What are neutrophil extracellular traps (NETs)

A

Release of DNA webs decorated with all 5 histones and neutrophil derived granular proteins with antimicrobial activity
(Slide 24)

43
Q

What can neutrophil extracellular traps (NETs) cause?

A

Immobilisation of bacteria at the site of infection
(Slide 24)

44
Q

What is NETosis?

A

A specialised type of apoptosis caused by neutrophil extracellular traps (NETs)
(Slide 24)

45
Q

What is tuberculosis caused by?

A

Mycobacterium tuberculosis (Mtb)
(Slide 28)

46
Q

What type of pathogen is mycobacterium tuberculosis?

A

Intra-macrophage
(Slide 28)

47
Q

What is important in limiting the ability of the mycobacterium tuberculosis to invade macrophages?

A

Innate immunity
(Slide 28)

48
Q

What 2 cells release TNF-α to induce apoptosis of macrophages infected with tuberculosis?

A

Natural killer and cytotoxic T cells
(Slide 28)

49
Q

What are 3 ways to limit tuberculosis?

A

Macrophage stimulation - to kill bacterium
Apoptosis of infected macrophage
Granuloma - multicellular structures to limit mycobacterium tuberculosis growth
(Slide 28)

50
Q

What do macrophages infected with virulent (severe) mycobacterium tuberculosis (Mtb) secrete more of?

A

IL-10
(Slide 29)

51
Q

What 2 things result from macrophages infected with virulent Mtb secreting more IL-10?

A

IL-10 downregulates activity of macrophages - so less NO etc produced - switching off macrophage killing mechanisms
IL-10 induces release of TNFR-2 which forms a complex with TNF-α and downregulates TNF-α induced apoptosis of macrophages - causing survival of Mtb infected macrophages
(Slide 29)

BM 212: Introduction to Immunology (13 decks)

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