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Phase 2a > ICS - Immunology 2 > Flashcards

ICS - Immunology 2 Flashcards

1
Q

Haematopoiesis starts with…?

A

Multi potential hematopoietic stem cell (hemocytoblast)

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2
Q

What do hemocytoblasts differentiate into?

A
  • Common myeloid progenitor- Common lymphoid progenitor
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3
Q

What do common myeloid progenitors differentiate into?

A
  • Megakaryocytes (—> thrombocytes)- Erythrocytes- Mast cells- Myeloblast (—> basophil, neutrophil, eosinophil, monocyte (—> macrophage))
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4
Q

What do common lymphoid progenitors differentiate into?

A
  • Natural killer cell- Small lymphocyte (—> T lymphocyte, B lymphocyte (—> plasma cell))
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5
Q

Describe innate immunity

A
  • Rapid and non-specific defence system- Present from birth- Focused around physical and chemical barriers - No lymphocyte involvement
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6
Q

Give examples of physical and chemical barriers used in innate immunity

A

Skin, mucociliary escalator, gastric acid, hairs, lysozymes

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7
Q

What do lysozymes do?

A

Destroys bacterial cell walls

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8
Q

When do monocytes become macrophages?

A

When they migrate from blood to tissue

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9
Q

Describe the role of neutrophils

A

Phagocytosis and bactericide

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10
Q

Describe the role of macrophages

A

Phagocytosis, antigen presenting and cytokine secretion

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11
Q

Describe the role of basophils

A

Secrete histamine and heparin in allergic reactions, eczema, hayfever etc.

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12
Q

Describe the role of eosinophils

A

Release cationic granules in parasitic infections

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13
Q

Describe the role of mast cells

A

Release histamines when IgE binds to them during anaphylaxis and asthma (type 1 hypersensitivity reactions)

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14
Q

Describe the role of natural killer cells

A

Release lytic granules that kill virus infected cells

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15
Q

Describe the role of dendritic cells

A

Antigen presenting cells that reside in the epithelium (liver = kupffer, skin = langerhans)

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16
Q

Describe the role of antigen presenting cells

A

Process and present antigens from pathogens for recognitions

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17
Q

What are the main antigen presenting cells (considered ‘professional’ at activating lymphocytes)?

A

Dendritic cells (also macrophages and B cells)

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18
Q

How are bacteria/fungi destroyed?

A

Phagocytosis

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19
Q

How are viruses destroyed?

A

Cellular shutdown/resistance and apoptosis

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20
Q

Which leukocytes are polymorphonuclear?

A

Neutrophils, basophils and eosinophils

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21
Q

Which leukocytes are mononuclear?

A

Monocytes, B lymphocytes and T lymphocytes

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22
Q

Where do T cells mature?

A

Thymus

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23
Q

Where do B cells mature?

A

Bone marrow

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24
Q

How do T cells recognise antigens?

A

T cells cannot recognise soluble antigens. Antigens must be displayed by an APC and bound to MHC1/2 in order to be recognised

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25
Q

What do pattern recognition receptors (PRRs) include?

A

Chemoattraction of leukocytes and phagocytosis

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26
Q

What are pattern recognition receptors (PRRs)?

A

Receptors on cells that bind to PAMPs on microbes. They recognise patterns that belong to non-self organisms

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27
Q

PRRs and PAMPs are associated with what kind of immunity?

A

Innate immunity

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28
Q

What are toll-like receptors?

A

A class of PRRs that recognise both invading pathogens and endogenous molecules released from dying cells and damaged tissue (DAMPs). Send signals to the nucleus to secrete cytokines and interferons

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29
Q

What does TLR2 recognise?

A

Foreign substances

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30
Q

What does TLR4 recognise?

A

Gram-negative lipopolysaccharide

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31
Q

What does TLR5 recognise?

A

Flagellin

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32
Q

What does TLR7 recognise?

A

Single-stranded RNA

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33
Q

What does TLR9 do?

A

Binds DNA present in bacteria/viruses and triggers signalling cascade that lead to a pro-inflammatory cytokine response

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34
Q

Where are complement system plasma proteins derived from?

A

The liver

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35
Q

What are the 3 main outcomes of the complement system activation?

A
  1. Opsonisation (C3b and C4b) - increased phagocytosis2. Chemotaxis (C3a and C5a) - attracts and activates leukocytes3. Direct lysis (C5 to C9) - kill cell directly
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36
Q

What are the 3 pathways of the complement system?

A
  1. Classic2. Alternative3. Lectin
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37
Q

What activates the classic pathway of the complement system?

A

Antibodies

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38
Q

What activates the alternative pathway of the complement system?

A

Bacterial cell walls and endotoxin

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39
Q

What activates the lectin pathway of the complement system?

A

Mannose binding protein

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40
Q

What are pathogen associated molecular patterns (PAMPs)?

A

Patterns/structures of molecules found on microbes, specific to microbes

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41
Q

Give 4 examples of pathogen associated molecular patterns (PAMPs)

A
  1. Flagellin - protein found in bacterial flagella2. Lipopolysaccharide (LPS) - found in outer membrane of gram-negative bacteria3. Peptidoglycan - found in bacterial cell walls4. Lipoarabinomannan - mycobacteria
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42
Q

What happens when a PAMP binds to a PRR?

A

The innate immune response and inflammatory response is triggered

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43
Q

Define adaptive immunity

A

Specific acquired defence system. Has a memory and quicker response

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44
Q

What is the function of T helper 1 (CD4)?

A

Involved in cell-mediated immunity (response against intracellular pathogens). Regulates monocytes and macrophages and secretes cytokines. Secrete interferon gamma which causes cells to undergo apoptosis

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45
Q

What is the function of T helper 2 (CD4)?

A

Involved in humoral immunity (response against extracellular pathogens). Regulates eosinophils, basophils and mast cells and secretes cytokines. Binds to B cells and triggers them to divide

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46
Q

What is the function of T reg?

A

Regulates immune response

47
Q

What is the function of Th17?

A

Protection against extracellular pathogens. TH17 cells produce transcription factors and cytokines that suppress T reg cells

48
Q

What is the function of cytotoxic T cells (CD8)?

A

Bind to antigens and release perforin (causes cell lysis) and granzymes (induces apoptosis). Also secrete molecules that stop neighbouring cells from become infected and pro-inflammatory molecules/chemokines that attract other immune cells to the site of infection

49
Q

What is the function of B cells?

A

Become plasma cells which secrete antibodies

50
Q

Give 3 functions of antibodies

A
  1. Neutralise toxins2. Opsonisation3. Activate classic complement system
51
Q

What are the 5 main antibodies?

A

IgA, IgM, IgG, IgE and IgD

52
Q

Describe IgA

A
  • Found in colostrum (breast milk) and coats noenate gut- Found in mucous membranes (resp/digestive tract), saliva and tears
53
Q

Describe IgM

A
  • Found in blood and lymph fluid- First antibody made when fighting a new infection- Activates complement system
54
Q

Describe IgG

A
  • Found in blood (most abundant)- Important during secondary response- Can cross placenta (in utero protection)
55
Q

Describe IgE

A
  • Found in the blood (small amounts)- Bound to mast cells and basophils- Important in allergies
56
Q

What are the two most common antibodies?

A

IgG and IgM

57
Q

Describe primary immunodeficiency and give an example

A
  • Born with intrinsic defects in the immune system- Rare and mostly genetic disorders- e.g. SCID (severe combined immunodeficiency)
58
Q

Describe secondary immunodeficiency (a.k.a immunosuppression) and give an example

A
  • Acquired- Can be drug induced (e.g. steroids, azathioprine, chemotherapy)- e.g. AIDS (acquired immune deficiency syndrome)
59
Q

Describe type I hypersensitivity

A
  • IgE mediated-E.g. anaphylaxis- IgE binds to mast cells which leads to mast cell degranulation (release of histamine)- Can be caused by allergies
60
Q

Describe type II hypersensitivity

A
  • IgG mediated cytotoxicity- E.g. autoimmune haemolytic anaemia- Can be caused by transplant rejection
61
Q

Describe type III hypersensitivity

A
  • Immune complex deposition- Immune complexes not been adequately cleared- Gives rise to an inflammatory response- E.g. systemic lupus erythematosus- Can be caused by fungal
62
Q

Describe type IV hypersensitivity

A
  • T cell mediated- E.g. graft vs host disease, MS- Can be caused by tuberculosis
63
Q

Give 6 features of anaphylaxis

A
  1. Rapid onset2. Blotchy rash3. Swelling of face and lips4. Wheezing5. Hypotension6. Cardiac arrest (if severe)
64
Q

Describe the general structure of an antibody

A

Fc region at base and two Fab regions (makes Y shape)

65
Q

What is the function of the Fc region on an antibody?

A

Binds to Fc receptor on phagocyte/B cell to bring microbes in close proximity to WBCs

66
Q

What is the function of the Fab regions on an antibody?

A

Bind to epitopes on antigens (on microbes). Variable regions

67
Q

What are cytokines?

A

Small proteins that orchestrate and regulate an immune response. Can either be pro-inflammatory or anti-inflammatory

68
Q

Name 4 types of cytokines

A
  1. Interferones (IFN)2. Interleukins (IL)3. Colony stimulating factors4. Tumour necrosis factors
69
Q

Describe the role of interferons

A

Produce antiviral proteins that induce a state of antiviral resistance in uninfected cells

70
Q

Describe the role of interleukins

A

Cause cells to divide, differentiate and secrete factors. Can be pro- (IL1) or anti-inflammatory (IL10)

71
Q

Describe the role of colony stimulating factors

A

Cause division and differentiation of bone marrow stem cells (to make more leukocytes)

72
Q

Describe the role of tumour necrosis factors

A

Mediate inflammation and cytotoxic reactions

73
Q

What do chemokines do?

A

Attract leukocytes to sites of infection

74
Q

Define extravasation

A

Migration of leukocytes from the circulation into tissues where infection is occurring

75
Q

What is secreted at tissues to initiate extravasation?

A

TNF alpha by pro-inflammatory molecules (e.g. macrophages)

76
Q

What does TNF alpha do?

A
  • Causes surrounding cells to secrete chemokines (attract neutrophils) - Causes endothelium to become sticky using adhesion molecules (neutrophils can stick)
77
Q

Describe extravasation

A
  1. TNF alpha released2. Adhesion molecules and chemokines stimulated3. Neutrophils bind and start to roll4. Neutrophils become stuck to endothelium (adhesion molecules and integrins)5. Neutrophils migrate through endothelium into tissue6. Migrate up chemokine conc. gradient to site of infection
78
Q

What is the function of major histocompatibility complex (MHC)?

A

Displays fragments from pathogens for recognition by T cells

79
Q

Which cells express MHC1?

A

All nucleated cells

80
Q

Which cells express MHC2?

A

Antigen presenting cells e.g. macrophages, dendritic cells, B cells

81
Q

Intrinsic antigens are displayed by…?

82
Q

Extrinsic antigens are displayed by…?

83
Q

Which type of T cell binds to MHC1?

A

Cytotoxic T cells (CD8)

84
Q

Which type of T cell binds to MHC2?

A

T helper cells (CD4)

85
Q

What happens to T cells that recognise self?

A

Killed in utero

86
Q

What are T cell receptors (TCRs)?

A

Receptors that recognise foreign antigens but only when displayed by MHCs

87
Q

What is required for T cell activation?

A

CD28 on T cell must bind to CD80/CD86 on APC

88
Q

What happens after a T cell binds to a T cell receptor?

A

IL-2 is secreted and binds to IL-2R on T cells. This produces a positive feedback mechanism of division and differentiation

89
Q

What 2 routes can activated T cells take?

A

CD8 way or CD4 way (–> TH1 and TH2)

90
Q

What happens to B cells that recognise self?

A

Killed in bone marrow

91
Q

Define autoimmunity

A

The system of immune responses of an organism against its own health cells, tissues and other normal body constituents

92
Q

When do we gain natural active immunity?

A

After exposure to antigens from pathogens in the environment

93
Q

When do we gain artificial active immunity?

A

After being vaccinated

94
Q

When do we gain natural passive immunity?

A

From maternal antibodies in colostrum

95
Q

When do we gain active passive immunity?

A

After transfer of antibodies from one organism to another

96
Q

Define negative phase

A

Period after initial antigen exposure where ones’ immunity is lower than before encountering the antigen

97
Q

Compare active and passive immunisation

A

Active is more effective than passive and has a memory but has a lag period and negative phase which passive doesn’t

98
Q

What is a live vaccine?

A

Live pathogen is injected

99
Q

Give 2 examples of live vaccines

A

BCG (TB) vaccine and MMR vaccine

100
Q

Give 3 advantages of live vaccines

A
  1. Effective, prolonged and comprehensive2. Immunological memory produced3. Usually only 1 vaccine needed
101
Q

Give 2 disadvantages of live vaccines

A
  1. Infection may occur in immunocompromised patients2. Vaccines often needed to be refrigerated
102
Q

What is an inactive vaccine?

A

Inactivated pathogen is injected

103
Q

Give 2 advantages of inactivated vaccines

A
  1. No risk of infection2. Less difficulty to store
104
Q

Give 2 disadvantages of inactivated vaccines

A
  1. Weaker response (humoral response - lack of T cell involvement)2. Boosters often needed
105
Q

What is a subunit vaccine?

A

Only antigenic part injected

106
Q

Give 1 advantage of subunit vaccines

A

Lower infection risk (safer)

107
Q

Give 2 disadvantages of subunit vaccines

A
  1. Repeat jabs needed2. Adjuvants needed to produce a response
108
Q

What is an adjuvant?

A

A substance added to a vaccination to stimulate an immune response (e.g. toxoid, proteins etc.). Convince the immune system that the body is infected

109
Q

What is a DNA vaccine?

A

Gene from pathogen expressed in host cell to cause an immune response and lead to memory cell production

110
Q

What is a recombinant vector vaccine?

A

Imitates effects of infection with pathogen using non pathogenic organism

111
Q

What is a polysaccharide vaccine?

A

Composed of long chains of sugar molecules that make up the surface capsule of certain bacteria

112
Q

What diseases can polysaccharides vaccines be used to treat?

A
  • Pneumococcal disease- Salmonella typhi- Meningococcal disease
113
Q

What are DAMPs?

A

Damage associated molecular patterns - endogenous molecules released by damaged or dying cells

Phase 2a (29 decks)

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