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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
What are chemokines?
A type of cytokine which induces chemotaxis
26
What is chemotaxis?
The recruitment (movement) of leukocytes to the site of injury/infection for inflammation
27
What is the function of interferons?
To induce an antiviral response in uninfected cells to limit the spread of a virus
28
What do interleukins do?
Cause cell division, differentiation or factor secretion Pro or anti-inflammatory
29
What does tumour necrosis factor (TNF) do?
Mediates inflammation and cytotoxic reactions
30
What are the five classes of antibodies/immunoglobulins?
GAMED IgG IgA IgM IgE IgD
31
What is the Fc region of an antibody?
The constant region Binds to receptor or complement 2 heavy chains
32
What is the Fab region of an antibody?
Hyper variable regions Bind to specific antigen Light chains
33
What immune response is IgM involved in?
Primary immune response Less specific and makes initial contact with antigen
34
What immune response is IgG involved in?
Secondary immune response Very specific Marker of immunologic memory Provides immunity to neonate
35
Which antibody receptor do basophils and mast cells have?
IgE
36
What is hypersensitivity?
The overreaction of the immune system to a stimulus
37
Describe Type I Hypersensitivity
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
Describe Type II hypersensitivity reactions
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
Describe Type III Hypersensitivity reactions
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
Describe Type IV hypersensitivity reactions
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
Give an example of a Type I hypersensitivity reaction
Anaphylaxis Eczema
42
Give an example of a Type II hypersensitivity reaction
Acute Haemolytic transfusion reactions, Goodpasture’s syndrome (destruction of glomerular basement membrane), haemolytic disease of newborn, rheumatic fever etc
43
Give an example of a Type III hypersensitivity reaction
Rheumatoid arthritis, Farmer’s lung
44
Give an example of a Type IV hypersensitivity reaction
Contact dermatitis, T1 Diabetes Mellitus, Mantoux test for TB, Coeliac disease, Hashimoto’s thyroiditis, Multiple Sclerosis
45
What is an allergen?
An antigen that triggers an allergic reaction
46
What is atopy?
An inherited trait for hypersensitivity
47
What do pattern recognition receptors (PRRs) on cells bind to when sensing microbes?
Pathogen-Associated Molecular Patterns (PAMPs) on the microbe
48
What are the types of PRR?
Lectin receptors Scavenger receptors Toll-Like Receptors (TLRs)
49
Name some subtypes of Toll-Like Receptors and what they bind to
TLR 2 - gram positive bacteria TLR 4 - gram negative bacteria TLR 5 - flagella TLR 7 - single stranded RNA TLR 9 - nonmethylated DNA
50
What does PRR activation trigger?
Innate immune response
51
What does the Major Histocompatability complex do?
Displays self/non-self antigens and initiates the T cell response Two classes
52
What is a class 1 MHC?
Displayed on all cells except red blood cells Involves intracellular/intrinsic pathogen (e.g. virus) CD8 cells directly kill infected cell
53
What is a class II MHC?
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
What is autoimmunity?
When components of the immune system start to recognise self antigens leading to immune responses
55
Give some examples of autoimmune conditions
Type 1 diabetes Mellitus Myasthenia gravis Graves’ disease Goodpasture’s syndrome Autoimmune thrombocytopenia Pernicious anaemia
56
What is immunodeficiency?
Full or partial impairment of the immune system
57
Give an example of an immunodeficiency condition
Primary: B cell, T cell, Severe Combined Immunodeficiency (SCID) Secondary (illness/environmental): malnutrition, medications like chemotherapy, chronic infections like HIV/AIDS
58
What is cancer immunoediting?
The immune system induces genetic changes to the tumour, resulting in tumour escape and recurrence but it can also kill it Two parts
59
What are the two parts of cancer Immunoediting?
Immunosurveillance, tumour progression
60
What is cancer immunosurveillance?
The immune system can recognise and destroy newly transformed/neoplastic cells Natural tumour immunity
61
What is tumour progression?
Increased growth speed and invasiveness of tumour Tumour becoming more aggressive and acquiring malignant potential
62
What are the two types of tumour antigens?
Tumour specific antigens (TSA) Tumour associated antigens (TAA)
63
What are tumour specific antigens?
Antigens only found on the tumour The result of point mutations or gene alterations
64
What are tumour associated antigens?
Antigens found on normal and tumour cells They are overexpressed on cancer cells
65
What is tumour escape?
When the immune response causes the tumour to change so that it won't be seen by the immune system
66
What is Immune evasion?
When tumours change the immune response by promoting immune suppressor cells
67
What are the three types of cancer immunotherapy?
Active, passive, cell-based
68
Describe active cancer immunotherapy
A vaccine against a cancer Could be killed tumour, purified tumour, professional APC-based, DNA or viral vaccine
69
Describe passive cancer immunotherapy
- Adoptive cellular therapy (T cells specific to that tumour) - Anti-tumour antibodies - These don't kill the tumour directly
70
Describe cell-based cancer immunotherapy
Activates the patient's immune system to attack the tumour It also acts as delivery vehicles to target therapeutic genes at cancer
71
Why do hypoxic tumour cells have a poor prognosis?
- 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
How can we treat hypoxic tumours?
Macrophages can deliver cancer-killing viruses to the tumour which then destroys it
73
What is passive immunity?
'Pre-formed' immunity administered from one person or animal to another
74
Describe passive immunity
Only antibody mediated Gives immediate protection Short-lived (no immunologic memory)
75
Give some examples of passive immunity
Placental antibodies Human tetanus Ig Human rabies specific Ig Human Hepatitis B Ig Varicella Zoster Ig
76
What type of immunisation is vaccination?
Active
77
What are the three main types of vaccines?
Whole (killed or live-attenuated) Subunit (the part that triggers immune response) Genetic material
78
What are the pros of whole killed vaccines?
No infection risk Storage is easier
79
What are the cons of whole killed vaccines?
They only activate the humoral response The immune response can be weaker without infection Booster vaccines are normally required
80
Give some examples of whole killed vaccines
Anthrax, cholera, Hep A
81
What are the pros of whole live attenuated vaccines?
Transient infection Full, natural immune response activated B and T cell memory Normally only requires single dose
82
What are the cons of whole live attenuated vaccines?
Chance of infection in immunocompromised patients Refrigeration needed for transport and storage
83
Give some examples of whole live attenuated vaccines
BCG (TB), polio, typhoid, mumps
84
What are the pros of subunit vaccines?
No infection risk Theoretically safer than whole pathogens Easier storage and preservations
85
What are the cons of subunit vaccines?
Less powerful immune response than live attenuated vaccines Need repeat vaccinations
86
What are the pros of DNA vaccines?
Storage is easier Immune response is similar to a natural infection and leads to B and T cell memory
87
What are the cons of DNA vaccines?
No transient infection Mild immune response so requires boosting

Phase 2a (9 decks)

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