Block C Part 2: Immunology Flashcards

1
Q

Is innate immunity specific or non-specific?

A

Non- Specific
(Lecture 2, Slide 3)

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2
Q

How is innate immunity acquired?

A

It is inherited
(Lecture 2, Slide 3)

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3
Q

What is the purpose of innate immunity?

A

It protects against foreign cells or substances without having to recognize their specific identity
(Lecture 2, Slide 3)

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4
Q

How does innate immunity protect against foreign cells?

A

It recognizes a general, conserved property that marks an invader as foreign
(Lecture 2, Slide 3)

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5
Q

Does innate immunity require prior exposure to invaders?

A

No
(Lecture 2, Slide 3)

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6
Q

What is the initial line of defence of innate immunity?

A

The body surface
(Lecture 2, Slide 4)

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7
Q

How do skin glands protect against foreign invaders?

A

They secrete antimicrobial molecules (mild acids and enzymes)
(Lecture 2, Slide 4)

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8
Q

How does mucus protect against foreign invaders?

A

It is sticky to trap invaders and is antimicrobial
(Lecture 2, Slide 4)

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9
Q

How does stomach acid protect against foreign invaders?

A

It destroys invaders
(Lecture 2, Slide 4)

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10
Q

What is endocytosis?

A

When phagocytes engulf and destroy particles
(Lecture 2, Slide 5)

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11
Q

What are 6 types of leukocytes?

A

Neutrophils, eosinophils, monocytes, macrophages, basophils and natural killer cells
(Lecture 2, Slide 5)

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12
Q

What do natural killer cells do?

A

They recognize general features of cancer or virus-infected cells as part of non-specific immunity and kill them
(Lecture 2, Slide 5)

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13
Q

What do dendritic cells do?

A

They perform macrophage functions
(Lecture 2, Slide 5)

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14
Q

What do mast cells release?

A

Histamine
(Lecture 2, Slide 5)

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15
Q

What is inflammation?

A

It is a innate local response to infection or injury
(Lecture 2, Slide 7)

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16
Q

What are the 3 purposes of inflammation?

A

Destroys or inactive foreign invaders, clears area of dead cells and sets stage for tissue repair
(Lecture 2, Slide 7)

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17
Q

What are the 5 key cellular components of inflammation?

A

Phagocytes, neutrophils, macrophages, dendritic cells, and mast cells
(Lecture 2, Slide 7)

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18
Q

What is inflammation induced and regulated by?

A

Cytokines
(Lecture 2, Slide 7)

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19
Q

What induces vascular changes?

A

Inflammatory signals secreted by injured tissue, mast cells and neutrophils
(Lecture 2, Slide 8)

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20
Q

What are 2 ways in which vascular changes affect the body?

A

It increases blood flow to area which increases delivery of beneficial proteins and leukocytes (white blood cells)
Increases vascular permeability allows plasma proteins to gain entry to interstitial fluid.
(Lecture 2, Slide 8)

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21
Q

What releases inflammatory mediators?

A

Phagocytes
(Lecture 2, Slide 8)

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22
Q

What do inflammatory mediators do?

A

They bring in more phagocytes into the area
(Lecture 2, Slide 8)

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23
Q

How does scar tissue form?

A

Tissue repair isn’t always perfect and may leave scar tissue
(Lecture 2, Slide 8)

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24
Q

What are Interferon and Complement?

A

Antimicrobial proteins
(Lecture 2, Slide 10)

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25
Q

What does interferon do?

A

It inhibits viral replication without being specific to a particular virus
(Lecture 2, Slide 10)

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26
Q

How does Complement kill microbes?

A

It uses membrane attack complex (MAC) to create channels in microbial plasma membrane, causing microbes to burst
(Lecture 2, Slide 10)

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27
Q

What does PAMP stand for?

A

Pathogen-associated molecular pattern
(Lecture 2, Slide 11)

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28
Q

What does innate immunity depend on?

A

Recognition of general molecular features common to many types of pathogens or PAMPs
(Lecture 2, Slide 11)

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29
Q

Where are toll proteins found?

A

In the membranes of macrophages, dendritic cells and other immune cells
(Lecture 2, Slide 12)

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30
Q

What is the function of Toll proteins?

A

Recognise and bind to ligands with PAMPs
(Lecture 2, Slide 12)

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31
Q

What happens when a Toll protein on an immune cell binds to a PAMP ligand and what does this trigger?

A

Second messengers are generated, triggering cytokine secretion
(Lecture 2, Slide 13)

32
Q

Why are is the Toll protein family referred to as “TLRs”, and what does this stand for?

A

TLRs stands for “Toll-like receptors” and toll proteins are called this as many are membrane-bound receptors.
(Lecture 2, Slide 13)

33
Q

Is acquired immunity specific or non-specific?

A

Specific
(Lecture 2, Slide 15)

34
Q

What is the definition of an antigen?

A

Any molecule that the host does not recognize as itself
(Lecture 2, Slide 15)

35
Q

Does acquired immunity require exposure to foreign substances?

A

Yes
(Lecture 2, Slide 15)

36
Q

Where are Lymphocytes found?

A

They circulate in blood but most of them reside in organs of the lymphatic system
(Lecture 2, Slide 16)

37
Q

What does a network of lymphatic vessels do?

A

Collect lymph and returns the fluid to blood plasma
(Lecture 2, Slide 16)

38
Q

What are the 2 purposes of Primary lymphoid organs?

A

Site where lymphocytes differentiate into mature immune cells.
Supply mature lymphocytes to secondary lymphoid organs where the lymphocytes multiply
(Lecture 2, Slide 16)

39
Q

How do lymphocytes increase the chance they will encounter their antigen?

A

They circulate through lymphoid organs, interstitial fluid and then back to the lymphatic system.
(Lecture 2, Slide 16)

40
Q

Where do B cells mature?

A

In the bone marrow.
(Lecture 2, Slide 18)

41
Q

What do some B cells form?

A

Plasma cells
(Lecture 2, Slide 18)

42
Q

What kind of immunity do B cells have?

A

Humoral immunity
(Lecture 2, Slide 18)

43
Q

Where do T cells mature?

A

The thymus gland
(Lecture 2, Slide 19)

44
Q

What is the function of Cytotoxic T cells?

A

They directly kill infected, mutated, or transplanted cells
(Lecture 2, Slide 19)

45
Q

What is the function of helper T cells?

A

They assist in activating B cells and cytotoxic T cells
(Lecture 2, Slide 19)

46
Q

What immunity do T cells have?

A

Cell-Mediated immunity
(Lecture 2, Slide 19)

47
Q

What is the first stage of acquired immune response?

A

Recognition of antigen
(Lecture 2, Slide 22)

48
Q

What happens during the development of stage one of the acquired immune response?

A

Each lymphocyte synthesizes a membrane receptor that can bind to a specific antigen
(Lecture 2, Slide 22)

49
Q

How are antigens recognized by the lymphocyte during stage 1 of the acquired immune response?

A

Antigens bind to a lymphocyte receptor and are then recognized by the lymphocyte
(Lecture 2, Slide 22)

50
Q

How many antigens can a lymphocyte specify for?

A

1
(Lecture 2, Slide 22)

51
Q

What is the second stage of the acquired immune response?

A

Activation of Lymphocytes
(Lecture 2, Slide 23)

52
Q

How are clones made during stage 2 of the acquired immune response?

A

Upon binding of the antigen, lymphocyte undergoes cell division to make clones
(Lecture 2, Slide 23)

53
Q

What 2 things do lymphocyte clones function as in stage 2 of the acquired immune response?

A

Plasma cells that carry out the attack and memory cells for future attacks
(Lecture 2, Slide 23)

54
Q

What is the third stage of the acquired immune response?

A

Attack against the antigen
(Lecture 2, Slide 24)

55
Q

What do activated B cells differentiate into in stage 3 of the acquired immune response and what do these secrete?

A

They differentiate into plasma cells secreting antibodies
(Lecture 2, Slide 24)

56
Q

How are plasma cells and cytotoxic T cells killed after stage 3 of the acquired immune response and why?

A

They die by apoptosis to prevent excessive immune response
(Lecture 2, Slide 24)

57
Q

What is the purpose of memory cells?

A

Memory cells persist, awaiting future invasions by the same pathogen so that the body can respond quicker with antibodies as it recognises the pathogen immediately
(Lecture 2, Slide 24)

58
Q

What is Immunoglobulin (Ig) protein family composed of?

A

4 interlinked polypeptides
(Lecture 2, Slide 26)

59
Q

What 5 classes of immunoglobulin antibodies do mammals have?

A

IgA, IgD, IgE, IgG and IgM
(Lecture 2, Slide 26)

60
Q

What is the function of IgM and IgG?

A

They provide the bulk of specific immunity against bacteria and viruses in extracellular fluid
(Lecture 2, Slide 27)

61
Q

What is the function of IgE?

A

They participate in defences against multicellular parasites and allergic responses
(Lecture 2, Slide 27)

62
Q

What is the function of IgA?

A

It is secreted by plasma cells in the linings of gastrointestinal , respiratory and genitourinary tracts to act locally
(Lecture 2, Slide 27)

63
Q

What does the variable region in a B cell do?

A

It specifically recognizes the antigen
(Lecture 2, Slide 28)

64
Q

What is opsonization?

A

Antibodies link pathogen to nonspecific immune cell to trigger attack
(Lecture 2, Slide 29)

65
Q

What is cell mediated immunity?

A

It is an immune response not involving antibiotics
(Lecture 2, Slide 31)

66
Q

What happens during T cell maturation?

A

There are multiple DNA arrangements during T-cell maturation.
(Lecture 2, Slide 31)

67
Q

Can T-cells combine with antigens?

A

Not unless complexed with MHC class I receptor
(Lecture 2, Slide 31)

68
Q

What does MHC stand for?

A

Major histocompatibility complex
(Lecture 2, Slide 32)

69
Q

What is a MHC?

A

A MHC is a cellular “identity tag” - a genetic marker to identify self
(Lecture 2, Slide 32)

70
Q

Where are Class I MHCs found?

A

Found on all body cells except erythrocytes (red blood cells)
(Lecture 2, Slide 32)

71
Q

Where are Class II MHCs found?

A

Found only on antigen-presenting cells (APCs), macrophages, B cells, and dendritic cells
(Lecture 2, Slide 32)

72
Q

How are microbes phagocytized into fragments or epitopes?

A

By macrophages
(Lecture 2, Slide 33)

73
Q

What happens to microbe fragments?

A

They get complexed with MHC I and sent to the plasma membrane, where cytotoxic T cell binds to the complex and releases chemicals that kill the infected or cancerous cell
(Lecture 2, Slide 36)

74
Q

How do activated helper T cells help cytotoxic T cells to proliferate?

A

They release cytokines
(Lecture 2, Slide 37)

75
Q

What does perforin do to a target cell?

A

It causes it to burst
(Lecture 2, Slide 37)