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Year 2 EMS MoD > Immune Response and Hypersensitivity > Flashcards

Immune Response and Hypersensitivity Flashcards

1
Q

What are the 2 main subdivisions of the immune system?

A

Innate and adaptive.

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2
Q

What is innate immunity?

A

Non-specific defence mechanisms (e.g. skin, chemicals, immune cells).
-fast action

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3
Q

What are the main subdivisions of the innate immune system? (3)

A
  • Barrier and chemical mechanisms (e.g. skin)
  • Pattern recognition receptor (PRR)
  • Cellular (phagocytes, NK cells)
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4
Q

What is adaptive immunity?

A

Antigen-specific immune response.

-slower repsonse

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5
Q

What are the main subdivisions of the adaptive immune system? (2)

A
  • Humoral

- Cellular

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6
Q

What is humoral immunity?

A

Immunity mediated by macromolecules ( not cells) found in ECF such as secreted antibodies and complement proteins.

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7
Q

What are the main components of the innate immune system? (5)

A
  • PRR
  • Antimicrobial peptides
  • Cells
  • Complement components
  • Cytokines
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8
Q

What are pattern recognition receptors (PRR)?

A

Antigen recognition receptors in the innate system.

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9
Q

Are PRRs identical?

A

No, there’s a diversity of type, but each cell carries identical receptors of a given type.

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10
Q

What do PRRs commonly recognise? (2)

A
  • Pathogen-associated molecular patterns (PAMPs)

- Danger associated molecular patterns (DAMPs)

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11
Q

What are the 2 groups of PRRs?

A
  • Transmembrane (cell suraface) and intracellular

- Fluid-phase soluble molecules

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12
Q

Pattern recognition receptors:

What molecule does TLR4 recognise?

A

LPS.

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13
Q

Pattern recognition receptors:

What molecule does TLR5 recognise?

A

Flagellin.

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14
Q

Pattern recognition receptors:

What molecule does TLR9 (intracellular) recognise?

A

MyD88.

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15
Q

What are antimicrobial peptides (AMPs)?

A

Proteins produced in secretions&raquo_space; break down proteins in microbes.

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16
Q

Give some examples of antimicrobial peptides.

A

Defensins
Protegrin
Granulysin
Histatin

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17
Q

Give some examples of cells that play a role in the innate immune system.

A 
Macrophages
Dendritic cells
NK cells
Neutrophils
Eosinophils
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18
Q

What are the complement components of the innate immune system?

A
  • Classic and alternative complement pathway.

- Proteins that bind components

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19
Q

What are cytokines?

A

Molecules that mediate host defence and inflammation, and regulate the adaptive immune response.
-autocrine/paracrine/endocrine

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20
Q

What does autocrine mean?

A

Relating to a cell-produced substance that has an effect on the cell by which it is secreted.

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21
Q

What does paracrine mean?

A

Relating to a hormone which has effect only in the vicinity of the gland secreting it.

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22
Q

What does endocrine mean?

A

Relating to glands which secrete hormones or other products directly into the blood.

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23
Q

What is a fluid-phase recognition molecule?

A

Collectins.

  • C-type lectin family
  • Mannan-bindng lectin
  • Surfactant protein A / D
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24
Q

What is the function of fluid-phase recognition molecules? (3)

A
  • Recognise carbohydrates
  • Neutralisation of pathogens
  • Recruitment of adaptive response
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25
Q

What do fluid-phase recognition molecules bind via?

A

Carbohydrate-recognition domains (CRDs).

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26
Q

How many carbohydrate-recognition domains does mannose-binding lectin have?

A

2-6 clusters.

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27
Q

What are the main innate immune pathways? (3)

A
  • Classical
  • Mannose-binding lectin
  • Alternative
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28
Q

What is the role of IL1?

A

Initial cytokine&raquo_space; unwell, muscle ache, etc.

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29
Q

What does IL1 target? (3)

A
  • Endothelia
  • Hepatocytes
  • Hypothalamus
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30
Q

When are TNF and IL6 produced?

A

Early infection.

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31
Q

What does TNF target? (4)

A
  • Endothelia
  • Hepatocytes
  • Hypothalamus
  • Neutrophils
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32
Q

Adaptive immune response; what happens when a lymphocyte comes into contact with its specific antigen?

A

Clonal expansion.

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33
Q

What happens in primary lymphoid organs?

A

Lymphocytes develop and mature.

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34
Q

What are the primary lymphoid organs? (2)

A
  • Bone marrow (B cells)

- Thymus (T cells)

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35
Q

What happens in secondary lymphoid organs?

A

Initiate adaptive immune response and lymphocyte activation.

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36
Q

What are the secondary lymphoid organs? (3)

A
  • Spleen
  • Lymph nodes
  • Mucosal surfaces
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37
Q

What is the range of antigenic variability?

A

10^9.

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38
Q

How many genes does the human genome contain?

A

30,000.

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39
Q

How is diversity increased in human antigen receptors?

A

VDJ recombination.

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40
Q

What is the mechanism of antigen presentation?

A 
Antigens are internalised
>> broken down into peptides
>> peptides associated with class 2 molecules
>> brought to cell surface
>> activate helper T cells
>> these produce cytokines
>> B cells, T cells, etc.
41
Q

What are histocompatibility antigens?

A

Glycoproteins on mammalian cell surfaces.

-make us unique

42
Q

Where were histocompatibility antigens first found?

A

WBCs.

-ABO blood groups on RBCs

43
Q

What is another name for histocompatibility antigens?

A

Human leucocyte antigens (HLA).

  • determine blood group
  • used to match donors
44
Q

How many classes of histocompatibility antigens are there?

A

TWO;

  • class 1
  • class 2
45
Q

Name the class 1 histocompatibility antigens. (3)

A

HLA-A
HLA-B
HLA-C

46
Q

Name the class 2 histocompatibility antigens. (3)

A

HLA-DP
HLA-DQ
HLA-DR

47
Q

What are MHC proteins?

A

Cell surface proteins that present antigenic peptides to T cells.

48
Q

What type of T cell do MHC class 1 proteins present peptide to?

A

Cytotoxic T cells.

49
Q

What type of T cell do MHC class 2 proteins present peptide to?

A

Helper T cells.

50
Q

What is the function of B lymphocytes?

A

Produce and secrete antibodies.

-humoral immunity

51
Q

What is the function of cytotoxic T lymphocytes?

A

Kills infected/damaged cells.

-cellular immunity

52
Q

What is the function of helper T lymphocytes?

A

Secrete cytokines&raquo_space; control immune response.

-help B and T lymphocytes

53
Q

What is the function of suppressor T lymphocytes?

A

Dampen down the immune repsonse.

54
Q

How does binding of antibodies to antigens inactivate them? (4)

A

-Neutralisation
-Agglutination of microbes
-Precipitation of antigens
(these 3&raquo_space; PHAGOCYTOSIS)
-Activation of complement system
(»cell lysis)

55
Q

What is agglutination?

A

Clumping of particles.

56
Q

What protein secreted by cytotoxic T cells makes holes in the infected cell’s membrane.

57
Q

What is immunosuppression?

A

Reduced activation or efficacy of the immune system.

-can result in immunodeficiency

58
Q

What is immunodeficiency?

A

Lack of an efficient immune system-susceptibility to infections.

59
Q

What are the main uses of immunosupression? (3)

A
  • Transplant rejection
  • Autoimmune disease
  • Lymphoproliferative diseases
60
Q

What is hypersensitivity?

A

Undesirable, sometime fatal, reactions produced by normal immune system against innocuous antigens in a pre-sensitised host.

61
Q

What does innocuous mean?

A

Not harmful/offensive.

62
Q

What are the 4 types of hypersensitivity reactions?

A

I - IgE mediated
II - cytotoxic
III - immune complex
IV - cell mediated

63
Q

What is another name for a severe type 1 (IgE mediated) reaction?

A

Anaphylactic.

64
Q

What is the general process of a type I hypersensitivity reaction?

A

IgE mediated mast cell and basophil degranulation
» release of inflammatory mediators (e.g. histamine)
» and synthesis of lipid mediators (e.g. leukotrienes)

65
Q

What are the main clinical features of a Type I hypersensitivity reaction? (3)

A
  • Fast onset (15-30 mins)
  • Weal and flare
  • Can have 2nd phase response
66
Q

What are the common antigens associated with a Type I hypersensitivity reaction?

A
  • Pollen
  • Bee venom
  • Animal fur
67
Q

What common diseases are associated with Type I hypersensitivity reaction?

A
  • Hay fever
  • Allergic asthma
  • Dermatitis
  • Food allergies
68
Q

How is IgE produced?

A

By plasma cells under the control of IL-4 and CD40L-CD40 interaction.

69
Q

How high are IgE serum levels?

A

Extremely low.

-but high affinity receptor (FcR1) on mast cells and basophils

70
Q

What are the 2 types of response associated with Type I hypersensitivity reactions?

A
  • Early phase response

- Late phase response

71
Q

What is the general process of the early phase response?

A

Mast cell activation (FcR1)

|&raquo_space; degranulation (release of pre-formed mediators) and synthesis of lipid mediators.

72
Q

How are mast cells activated in Type I hypersensitivity reactions?

A

Cross-linking of FcR1 by allergen&raquo_space; activation.

73
Q

Name 3 common pre-formed mediators involved in Type I hypersensitivity reactions.

A
  • Histamine
  • Kallikrein
  • Tryptase
74
Q

What is the main action of histamine? (2)

A
  • Smooth muscle contraction

- Increased vascular permeability

75
Q

What is the main action of kallikrein?

A

Activate bradykinin.

-similar actions to histamine

76
Q

What lipid mediators are synthesised from arachidonic acid? (2)

A
  • Leukotrienes

- Prostaglandins (e.g. thromboxane)

77
Q

What are the main cells involved in the late phase response? (3)

A
  • Basophils
  • Eosinophils
  • T cells
78
Q

What is the role of basophils in the late phase response?

A

Similar to mast cells but over a longer time period.

-release of mediators

79
Q

What is the role of eosinophils in the late phase response?

A

Attracted to sites of allergic inflammation by chemokines
» release contents of granules (cytotoxic proteins)
» tissue damage

80
Q

What is the role of T cells in Type I hypersensitivity reactions?

A

Produce cytokines once activated.

-involved in both early and late phase responses

81
Q

What is a major source of pathogenesis in allergic responses?

A

Cytokine-driven activity.

82
Q

What type of reaction are Type II hypersensitivity reactions?

A

Antibody-mediated cytotoxic reactions.

83
Q

What is the process of Type II hypersensitivity reactions?

A

Antibodies bind to antigen on cell membrane;

  • activation of complement cascade&raquo_space; cell lysis
  • Aggregation of Fc portions&raquo_space; opsonisation/phagocytosis/destruction
84
Q

What are Type II hypersensitivity reactions initiated by? (2)

A
  • IgM

- complement-binding IgG

85
Q

Which is more efficient; IgM or IgG?

A

IgM.

-pentavalent

86
Q

Which requires multiple binding; IgM or IgG?

87
Q

What sort of cells are normally affected by Type II hypersensitivity reactions?

A

Haematopoietic cells.

88
Q

What common disorders are associated with Type II hypersensitivity reactions?

A
  • Blood group incompatibility
  • Autoimmune haemolytic anaemias
  • Affects neutrophils and platelets
89
Q

What sort of reactions are Type III hypersensitivity reactions?

A

Immune complex reactions.

90
Q

What is the general process of Type III hypersensitivity reactions?

A 
Ig + Ab = AgAb complex
>> FcR bind C1q
>> complement activation
>> C5a attracts neutrophils
>> C3b opsonin
>> phagocytosis of complexes (enzymes released)
>> TISSUE DAMAGE.
91
Q

What are the types of inactivation caused by antibody-mediated immunopathology? (3)

A
  • DIRECT (e.g. B12 deficiency)
  • INDIRECT (e.g. binding to hormones&raquo_space; AgAb complex clearance)
  • RECEPTOR BLOCKADE
92
Q

What sort of reactions are Type IV hypersensitivity reactions?

A

T cell mediated reactions.

93
Q

What is the general process of Type IV hypersensitivity reactions?

A

Initial perivascular infiltration of lymphocytes and monocytes
» Langerhan’s cells present antigen to T cells
» T cells release cytokines
» recruit macrophages
» TISSUE DAMAGE

94
Q

What do Type IV hypersensitivity reactions require?

A

Previous exposure to the antigen.

95
Q

Give an example of a skin condition caused by T cell mediated cytotoxicity (Type IV).

A

Contact dermatitis.
-Nickel, poison ivy
» DTH and cytotoxic reaction

96
Q

What type of hypersensitivity reaction causes granulomatous reactions?

A

Type IV hypersensitivity reactions.

97
Q

What are granulomas?

A

Collections of inflammatory cells (macrophages/lymphocytes) in tissues.
-IL2 release critical in initation of response

98
Q

What causes granulomatous diseases?

A
  • INFECTIONS (e.g. TB, leprosy)

- UNKNOWN (e.g. sarcoidosis, Crohn’s)

Year 2 EMS MoD (20 decks)

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