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Phase 2a > Immunology > Flashcards

Immunology Flashcards

1
Q

Describe the innate immune response

A
  • Instinctive, non-specific
  • Doesn’t depend on lymphocytes
  • No long term memory
  • Composed of physical and chemical barriers, phagocytic cells and complement
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2
Q

What are some physical and chemical barriers of the (innate) immune system

A

Skin,
Lysozymes in tears and other secretions,
Cilia and mucus in the bronchi,
Stomach acid,
Commensals in the GI tract, vagina and skin

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3
Q

How does inflammation help in the (innate) immune response?

A
  • Leukocyte recruitment
  • Kills pathogens
  • Neutralises toxins
  • Limits pathogen spread
  • Phagocytosis (clears pathogens and apoptotic debris)
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4
Q

Describe the adaptive immune response

A
  • Specific, acquired immunity
  • Requires lymphocytes and antibodies
  • Immunologic memory
  • Needs priming
  • Two types: cell-mediated and humoral
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5
Q

Describe cell-mediated immunity

A

Needs: Antigen Presenting Cells, T cells: CD4 (T helper) and CD8 (cytotoxic T cells), Major histocompatibility complex

T cells recognise foreign antigens
Use T cell receptors (TCRs) to recognise antigen presented in a MHC

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6
Q

Describe Humoral immunity

A

B cells
After the initial immune response they differentiate into plasma cells which act as the immunological memories and are specific to an antigen

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7
Q

Draw haematopoiesis

A
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8
Q

What are the three activation pathways of complement?

A

Classical - antibody bound to a microbe
Alternative - complement binds to a microbe
Lectin - mannose binds to lectin on a microbe

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9
Q

What does complement activation cause?

A

It causes the production of C3a, C3b and C5a proteins

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10
Q

What are the three ways that complement kills pathogens?

A

Chemotaxis - C3a and C5b are chemoattractors and bind to leukocytes to recruit them for inflammation
Opsonisation - C3b bind to microbe to make it more attractive for others to bind to
Direct lysis of microbes through membrane attack complex

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11
Q

Describe the membrane attack complex

A

Binds to a dimer and punches a hole in the pathogen’s membrane
This leads to osmolality out of the pathogen, killing it

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12
Q

Describe the process of phagocytosis

A
  1. Binding of phagocyte to microbe via a specific antigen on the phagocyte’s surface
  2. Engulfment of the microbe by the phagosome
  3. Phagolysosome formation (enzymes are secreted which kill the microbe)
  4. Secretion of molecule by the phagocyte to kill microbes outside of the cell
  5. Antigen presentation - the microbe’s antigens are presented on the surface of the phagocyte
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13
Q

Describe dendritic cells

A

The professional antigen presenting cell
Not haematopoietic
Found throughout the body

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14
Q

Describe Neutrophils

A

Key mediator of acute inflammation
Phagocytes
Granulocytes
Polymorphonuclear cells
Short life span

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15
Q

Describe eosinophils

A

Polymorphonuclear cells
Phagocytes
Granulocytes
Usually found in parasitic infections and hypersensitivity

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16
Q

Describe basophils

A

Granulocytes - granules contain histamine
Non phagocytes
Polymorphonuclear cells
Involved in hypersensitivity

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17
Q

Describe macrophages

A

Phagocytes
Antigen presenting cells
Have Toll-Like Receptors (TLRs), Complement receptors, antibodies

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18
Q

What is the function of macrophages?

A

The clearing or removal of foreign objects/pathogens
Clearing of apoptotic debris
Recruitment of other cells through cytokine release

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19
Q

Describe Natural Killer Cells

A

Target infected or cancerous cells
Kill cells using cytotoxic granules
Kill host’s natural cells rather than foreign cells

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20
Q

Describe B lymphocytes (B cells)

A

Involved in the humoral response
Phagocyte
Antigen Presenting Cell
Bind to specific antigens
Present to T cells causing T cell activation
Mature into plasma cells which secrete antibodies/immunoglobulins - immunologic memory

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21
Q

Describe T lymphocytes (T cells)

A

Involved in cell-mediated immunity
Recognise and bind to a specific antigen on APCs using T cell receptors (TCRs)
Two main types: CD4 and CD8

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22
Q

Describe CD4 cells

A

T helper cells
Secrete cytokines to help regulate immune response

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23
Q

Describe CD8 cells

A

T killer cells
Cytotoxic

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24
Q

What are cytokines?

A

soluble proteins secreted by macrophages or lymphocytes which act as stimulatory or inhibitory factors for cells

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25
Q

What are chemokines?

A

A type of cytokine which induces chemotaxis

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26
Q

What is chemotaxis?

A

The recruitment (movement) of leukocytes to the site of injury/infection for inflammation

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27
Q

What is the function of interferons?

A

To induce an antiviral response in uninfected cells to limit the spread of a virus

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28
Q

What do interleukins do?

A

Cause cell division, differentiation or factor secretion
Pro or anti-inflammatory

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29
Q

What does tumour necrosis factor (TNF) do?

A

Mediates inflammation and cytotoxic reactions

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30
Q

What are the five classes of antibodies/immunoglobulins?

A

GAMED
IgG
IgA
IgM
IgE
IgD

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31
Q

What is the Fc region of an antibody?

A

The constant region
Binds to receptor or complement
2 heavy chains

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32
Q

What is the Fab region of an antibody?

A

Hyper variable regions
Bind to specific antigen
Light chains

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33
Q

What immune response is IgM involved in?

A

Primary immune response
Less specific and makes initial contact with antigen

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34
Q

What immune response is IgG involved in?

A

Secondary immune response
Very specific
Marker of immunologic memory
Provides immunity to neonate

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35
Q

Which antibody receptor do basophils and mast cells have?

A

IgE

36
Q

What is hypersensitivity?

A

The overreaction of the immune system to a stimulus

37
Q

Describe Type I Hypersensitivity

A

IgE mediated
1. Sensitisation of mast cells
2. Re-exposure of sensitised mast cells to allergen
3. Early phase reactions (minutes): mast cell degranulation releasing histamine and tryptase
4. Late phase reactions: prolonged inflammatory response

38
Q

Describe Type II hypersensitivity reactions

A

Self-reactive B cells produce antibodies that bind to antigens on host cells
IgM and IgG mediated
Forms A-A complex at tissue site

39
Q

Describe Type III Hypersensitivity reactions

A

Mediated by immune complexes
Antibodies bind to antigens not bound to cell surface and then travel to target organ and cause damage
Immune complex formation activates complement

40
Q

Describe Type IV hypersensitivity reactions

A

Delayed reaction
APCs present antigen to CD4 cell
CD4 cell proliferates and differentiates into T helper cell
These travel to the tissue where the antigen originally presented and then release pro-inflammatory cytokines

41
Q

Give an example of a Type I hypersensitivity reaction

A

Anaphylaxis
Eczema

42
Q

Give an example of a Type II hypersensitivity reaction

A

Acute Haemolytic transfusion reactions, Goodpasture’s syndrome (destruction of glomerular basement membrane), haemolytic disease of newborn, rheumatic fever etc

43
Q

Give an example of a Type III hypersensitivity reaction

A

Rheumatoid arthritis, Farmer’s lung

44
Q

Give an example of a Type IV hypersensitivity reaction

A

Contact dermatitis, T1 Diabetes Mellitus, Mantoux test for TB, Coeliac disease, Hashimoto’s thyroiditis, Multiple Sclerosis

45
Q

What is an allergen?

A

An antigen that triggers an allergic reaction

46
Q

What is atopy?

A

An inherited trait for hypersensitivity

47
Q

What do pattern recognition receptors (PRRs) on cells bind to when sensing microbes?

A

Pathogen-Associated Molecular Patterns (PAMPs) on the microbe

48
Q

What are the types of PRR?

A

Lectin receptors
Scavenger receptors
Toll-Like Receptors (TLRs)

49
Q

Name some subtypes of Toll-Like Receptors and what they bind to

A

TLR 2 - gram positive bacteria
TLR 4 - gram negative bacteria
TLR 5 - flagella
TLR 7 - single stranded RNA
TLR 9 - nonmethylated DNA

50
Q

What does PRR activation trigger?

A

Innate immune response

51
Q

What does the Major Histocompatability complex do?

A

Displays self/non-self antigens and initiates the T cell response
Two classes

52
Q

What is a class 1 MHC?

A

Displayed on all cells except red blood cells
Involves intracellular/intrinsic pathogen (e.g. virus)
CD8 cells directly kill infected cell

53
Q

What is a class II MHC?

A

Only displayed on antigen presenting cells
Involves an extracellular/extrinsic pathogen
CD4 cell help B cells make antibodies and help kill cell directly as well as

54
Q

What is autoimmunity?

A

When components of the immune system start to recognise self antigens leading to immune responses

55
Q

Give some examples of autoimmune conditions

A

Type 1 diabetes Mellitus
Myasthenia gravis
Graves’ disease
Goodpasture’s syndrome
Autoimmune thrombocytopenia
Pernicious anaemia

56
Q

What is immunodeficiency?

A

Full or partial impairment of the immune system

57
Q

Give an example of an immunodeficiency condition

A

Primary: B cell, T cell, Severe Combined Immunodeficiency (SCID)
Secondary (illness/environmental): malnutrition, medications like chemotherapy, chronic infections like HIV/AIDS

58
Q

What is cancer immunoediting?

A

The immune system induces genetic changes to the tumour, resulting in tumour escape and recurrence but it can also kill it
Two parts

59
Q

What are the two parts of cancer Immunoediting?

A

Immunosurveillance, tumour progression

60
Q

What is cancer immunosurveillance?

A

The immune system can recognise and destroy newly transformed/neoplastic cells
Natural tumour immunity

61
Q

What is tumour progression?

A

Increased growth speed and invasiveness of tumour
Tumour becoming more aggressive and acquiring malignant potential

62
Q

What are the two types of tumour antigens?

A

Tumour specific antigens (TSA)
Tumour associated antigens (TAA)

63
Q

What are tumour specific antigens?

A

Antigens only found on the tumour
The result of point mutations or gene alterations

64
Q

What are tumour associated antigens?

A

Antigens found on normal and tumour cells
They are overexpressed on cancer cells

65
Q

What is tumour escape?

A

When the immune response causes the tumour to change so that it won’t be seen by the immune system

66
Q

What is Immune evasion?

A

When tumours change the immune response by promoting immune suppressor cells

67
Q

What are the three types of cancer immunotherapy?

A

Active, passive, cell-based

68
Q

Describe active cancer immunotherapy

A

A vaccine against a cancer
Could be killed tumour, purified tumour, professional APC-based, DNA or viral vaccine

69
Q

Describe passive cancer immunotherapy

A
  • Adoptive cellular therapy (T cells specific to that tumour)
  • Anti-tumour antibodies
  • These don’t kill the tumour directly
70
Q

Describe cell-based cancer immunotherapy

A

Activates the patient’s immune system to attack the tumour
It also acts as delivery vehicles to target therapeutic genes at cancer

71
Q

Why do hypoxic tumour cells have a poor prognosis?

A
  • Angiogenesis (blood supply can’t keep up with the growth rate of the tumour)
  • Immune suppression
  • Radio and chemotherapy resistant
  • It’s difficult to deliver drugs to these cells and the tumour can regrow afterwards
72
Q

How can we treat hypoxic tumours?

A

Macrophages can deliver cancer-killing viruses to the tumour which then destroys it

73
Q

What is passive immunity?

A

‘Pre-formed’ immunity administered from one person or animal to another

74
Q

Describe passive immunity

A

Only antibody mediated
Gives immediate protection
Short-lived (no immunologic memory)

75
Q

Give some examples of passive immunity

A

Placental antibodies
Human tetanus Ig
Human rabies specific Ig
Human Hepatitis B Ig
Varicella Zoster Ig

76
Q

What type of immunisation is vaccination?

A

Active

77
Q

What are the three main types of vaccines?

A

Whole (killed or live-attenuated)
Subunit (the part that triggers immune response)
Genetic material

78
Q

What are the pros of whole killed vaccines?

A

No infection risk
Storage is easier

79
Q

What are the cons of whole killed vaccines?

A

They only activate the humoral response
The immune response can be weaker without infection
Booster vaccines are normally required

80
Q

Give some examples of whole killed vaccines

A

Anthrax, cholera, Hep A

81
Q

What are the pros of whole live attenuated vaccines?

A

Transient infection
Full, natural immune response activated
B and T cell memory
Normally only requires single dose

82
Q

What are the cons of whole live attenuated vaccines?

A

Chance of infection in immunocompromised patients
Refrigeration needed for transport and storage

83
Q

Give some examples of whole live attenuated vaccines

A

BCG (TB), polio, typhoid, mumps

84
Q

What are the pros of subunit vaccines?

A

No infection risk
Theoretically safer than whole pathogens
Easier storage and preservations

85
Q

What are the cons of subunit vaccines?

A

Less powerful immune response than live attenuated vaccines
Need repeat vaccinations

86
Q

What are the pros of DNA vaccines?

A

Storage is easier
Immune response is similar to a natural infection and leads to B and T cell memory

87
Q

What are the cons of DNA vaccines?

A

No transient infection
Mild immune response so requires boosting

Phase 2a (9 decks)

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