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Immunology Flashcards

1
Q

What are the 2 types of acquired immunity?

What type of cell is responsible for each?

A

Humoral (Ab-mediated) - B cells

Cell-mediated - T cells

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2
Q

What can happen when the immune balance is tipped off?

A
  1. Over-reaction (Reaction to self/ Autoimmunity, Allergies)

2. Under-reaction: Infections, Cancer

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3
Q

When is natural and adaptive immunity present?

A

Natural: From birth
Adaptive: By presence of foreign materials; environment-dependent

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4
Q

How fast do innate and acquired immunity respond?

A

Innate: Rapid, first to respond (0-96hrs)
Acquired: Slow, lag time from exposure (>96hrs)

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5
Q

Which immunity has memory and is specific?

What does immunological memory help it to do?

A

Acquired immunity.
Memory allows it to respond faster and more powerfully subsequently
Specific and unique response to each antigen

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6
Q

What helps to self-regulate the acquired immune system?

A

Regulatory T-cells; to maintain tolerance to self-antigens, and has immunosuppressive function)

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7
Q

What does loss of tolerance to self-antigens result in?

A

Autoimmunity

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8
Q

Which immune system is able to discriminate from self and non-self?

A

Both

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9
Q

In the following immune cells and factors:
Macrophages, B cells, Mast cells, NK cells, Neutrophils, T cells, Antibodies, Complement.

Which immune system do they each fall under?

A

Innate: Macrophages, Mast cells, NK cells, Neutrophils, Complement

Acquired: B cells, T cells, Antibodies

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10
Q

What are 4 positive acute phase proteins and 2 negative acute phase proteins?

A

Positive: IgG, C3b, CRP, Mannose-binding lectin
Negative: Albumin, Transferrin (Values decreases when there is inflammation)

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11
Q

Which immune system does physical barriers fall under?

A

Innate

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12
Q

Which system does pathogen usually attack? (2)

A

Circulatory and lymphatic

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13
Q

What are physical/ structural factors of the skin as a natural barrier? (4)

A

Tightly packed
Multi-layered (Stratified squamous)
Highly keratinised
High turnover

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14
Q

What are 2 physiological factors of the skin for it to act as a natural barrier?

A

pH5.5 (Acidic) - Sweat, saliva, urine, gastric acid

Low O2 tension

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15
Q

What are 5 secretions of the skin to prevent pathogen entry?

A 
Hydrophobic oils from sebaceous glands
Ammonia
Enzymes (Lysozyme in tears and sweat to digest bacteria cell wall)
Defensins
Anti-microbial peptides (Directly kills)
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16
Q

Where does mucous membrane line?

A

Body CAVITIES in contact with environment

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17
Q

What are 3 components of the mucous membrane as a natural barrier?

A

Mucus - traps bacteria and removed by ciliated cells via sneezing/ coughing
Secretory IgA (DIMER): prevents attachment and penetration
Lactoferrin: starve pathogens of iron

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18
Q

Other than skin and mucous membrane, what else exists as part of the physical barrier as a first line of defence?

A

Commensal bacteria - competes with pathogen for resources

They also produce fatty acids and bactericidins

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19
Q

How do hair and earwax contribute to natural barrier?

A

Traps pathogens

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20
Q

What are 2 tissue-resident innate immune cells and what are their roles?

A
  1. Macrophages - bacteria killing, phagocytosis, antigen presentation (Pro-inflammatory), wound healing and tissue repair (anti-inflammatory)
  2. Mast cells - parasitic killing (pro-inflammatory)
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21
Q

What is the process of coating pathogens to enhance phagocytosis?
What are 3 factors that help coat?

A

Opsonisation.

Opsonins: IgM/G, C3b, CRP

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22
Q

What signature molecular motif do pathogens express and what receptors bind to these motifs? Which cell expresses these set of receptors?
What happens upon binding?

A

Pathogens express PAMPs
Macrophages have PRRs that binds to specific PAMPs

Cytoskeletal rearrangement -> phagosome formation -> fuse with late endosomes and lysosomes -> mature phagolysosomes -> killed internally and contents digested by proteases and hydrolyases

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23
Q

What happens to the degraded products in the phagolysosome?

A

Antigens - released into ECF

Pathogen-derived peptides - expressed on MHC-II molecules

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24
Q

What can induce phagocytosis? (2)

What are released in the process? What do they cause?

A

PAMPs and opsonin binding

Pro-inflammatory mediators causing localised, acute inflammation

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25
Q

5 examples of pro-inflammatory mediators

A

TNFa, NO, Prostaglandins, Leukotrienes, Histamines

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26
Q

What happens when parasites invade?

A

Too large to be phagocytosis thus:

Damaged cells send out danger signals to mast cells and/or PRR and PAMP binding –> activate –> degranulate (pre-formed pro-inflammatory substance released) and gene expression (produce new pro-inflammatory substance) –> extracellular pathogen killed

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27
Q

What are the 5 hallmarks of ACUTE inflammation?

A
  1. Redness - arteriole vasodilation, increased blood flow
  2. Oedema - increased post-capillary venule permeability and fluid accumulation in extravascular space
  3. Pain - stimulation of nerve endings
  4. Loss of function - due to pain and swelling
  5. Fever - temperature set point raised in hypothalamus
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28
Q

What are the 3 complement pathways?

A

Classical, Mannose-binding lectin, Alternative

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29
Q

What plasma cascade system produces protein to sustain vasodilation and other physical inflammatory effects?

A

Kinin system

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30
Q

What activates C5 convertase?

A

Active C3b on cell surface

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31
Q

What is formed at the last step of the complementary system?

A

MAC complex

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32
Q

How is C3 convertase activated in the mannose binding pathway?

A

Mannose-binding lectin (MBL) binds to mannose and peptidoglycan on bacteria causing MBL to change conformation and complex which then activate C3 convertase

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33
Q

What does the alternative complement pathway involve?

A

Amplication and positive feedback of C3 convertase by re-using C3b from cleaved C3

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34
Q

Why does C3b not causing any downstream complement effects on human cells?

A

Have inhibitory proteins against C3b

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35
Q

Does C5b or C5a go on to form the MAC?

A

C5b

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36
Q

What are anaphylatoxins? What are their effects (3)

A

C3a and C5a.
Changes local vasculature, acute inflammation and leukocyte recruitment by activating and degranulating mast cells an acting directly on local blood vessels

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37
Q

What vascular changes does inflammation promote?

A

Vasodilation of post-capillary venules thus losing tight junctions and causing redness and oedema

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38
Q

How are neutrophils (monocytes) recruited, activated/ mobilised during inflammation? (5)

A

Margination due to increased viscosity and slower flow AT POST-CAPILLARY VENULES
Binding to adhesion molecules on endothelial cells (Selections, ICAM-1)
Migration across endothelium via diapedesis
Movement within tissue via chemotaxis along chemotactic gradient
Neutrophils killing mechanism activated by PAMPs

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39
Q

How do neutrophils navigate within tissues?

A

Its integrins bind to extracellular matrix proteins

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40
Q

What promotes expression of Selectins on endothelial surface. What neutrophil movement does it cause?

A

Histamine and TNFa.

Weak binding to neutrophil surface causes it to roll along endothelium

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41
Q

What does ICAM-1 bind to? What is required for firm binding?

A

LFA-1 receptor
Chemokines from damaged cells needed to fully activate LFA-1 receptor to firmly bind to ICAM-1 for stable adhesion and aggregation

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42
Q

Neutrophil activation enhanced in presence of?

A

Pro-inflammatory mediators

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43
Q

LFA-1 deficiency is due to defective?

What mode of inheritence is this?

A

Defective CD18 - neutrophils cannot migrate out

Autosomal recessive

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44
Q

What are the 3 roles of neutrophils?

A

Phagocytosis
Degranulation
Neutrophil extracellular traps

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45
Q

How do neutrophils kill internalised pathogens? (2)

A
  1. Phagolysosomal killing - pH rise to activate antimicrobial response and pH drops for acid hydrolases to degrade bacterium
  2. ROS-dependent: NADPH-oxidase complex assemble to release ROS into phagolysosome
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46
Q

What damage does neutrophillic degranulation cause? (3)

What is it limited by? (1)

A

Directly kill nearby bacteria and fungi and causes bystander tissue damage
Limited by proteinase inhibitors

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47
Q

What induces Neutrophil extracellular traps?

What does NETs do?

A

Extracellular bacteria and fungi.
Release of intra-nuclear contents (DNA, histone, granular proteins, neutrophil elastase) to immobilise and trap pathogens to stop them from spreading.

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48
Q

What is the best antigen presenting innate immune cell?

A

Dendritic cell

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49
Q

What is the best innate immune cell for TNFa production, killing and degradation?

A

Neutrophil

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50
Q

How long is the T1/2 for CRP?

A

Short

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51
Q

Can viruses be phagocytosed?

A

No, too small for recognition

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52
Q

What do viral infected cells release? Are these virus specific?

A

IFNa/B.

No, they are host specific

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53
Q

What does IFNa/B signal neighbouring infected (1) and uninfected (3) cells to do?

A

Uninfected - destroy own RNA, slow protein synthesis and increase surface MHC I to activate T-cells
Infected - undergo apoptosis

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54
Q

What innate immune cell is activated during viral infection? How is it activated?

A 
NK cells (Longer lived Large granular lymphocytes)
Activated when MHC I is downregulated/ absent (in cancer/ pathogens) --> releases cytotoxic granules (perforins and granzymes) along with IFN-y and TNFa at close-proximity leading to apoptosis

**Lysis will lead to virion release

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55
Q

Other than responding to MHC I levels, what other pathogens do NK cells kill?

A

Ab-bound pathogens

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56
Q

Where do T-cells mature?

A

Thymus

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57
Q

What happens to B or T cells if they react to self-antigens in a normal immune system?

A

Destroyed or inactivated

58
Q

What kind of pathogens do B and T cells defend against?

A

B cells - extracellular and intracellular

T cells - intracellular

59
Q

What is an antibody made of?

A

2 heavy + 2 light polypeptide chains

60
Q

What do antibodies bind to?

A

1 specific antigenic epitope

*1 antigen has many antigenic epitopes

61
Q

How to distinguish between different classes of Ab?

A

By constant region of heavy chain

62
Q

What can membrane-bound Ab on B-cells do?

A

Act as B cell receptor (IgM or IgD) to bind to specific antigenic epitope

63
Q

Individual T/B cells express _ ____ type of antigen receptor which binds to only _ ____ antigenic epitope

A

1 specific

64
Q

What are the 5 secondary lymphoid tissues where B and T cells are usually activated by antigens?

A 
Lymph nodes - tissue infection
Spleen - blood borne infection
Mucosal-associated lymphoid tissue - throat/GI infections
Peyer's patches (Ileum)
Tonsils
65
Q

How do naive T and B cells enter LNs?

How long do they stay there?

A

Migrate trans-endothelially via high endothelial venules.

A few days

66
Q

How do lymph enter the lymph nodes?

A

Afferent lymphatics via high endothelial venules

67
Q

What are the 2 zones in the lymph nodes?

A

T cell zone - centre; paracortex

B cell zone (Germinal centre) - In stromal cells at the periphery follicles

68
Q

What kind of junctions do high endothelial venules have?

A

Permanent gap junctions and vasodilated

69
Q

If B and T cells do not encounter antigens in the lymph nodes, how do they return back to circulation?

A

Via medullary sinus –> efferent lymphatic vessel –> subclavian vein

70
Q

What happens when naive or memory B cells are activated?

A

Clonal proliferation and differentiation into 2 effector cells

  • Plasma cells - Short-lived (3-4 days), secrete soluble, antigen-specific antibodies, large in size due to highly active machinery
  • Memory B cells - long-lived
71
Q

What kind of BCRs do daughter cells express?

A

BCR with same antigen-specificity as parent B cell

72
Q

What do highly proliferative cells form within the B cell zone (Germinal centre)?

A

Secondary follicle

73
Q

How many signals are needed to fully activate a naive/ memory B cells?
What are these signals? (4)

A

2.

Antigen bound to BCR
Helping signals from Th cells
Signal 1 from BCR + Signal 2 from PRR + PAMP
Antigen with repetitive antigenic epitopes (e.g. peptidoglycan) - Signal 1 + 2 from multiple BCRs

74
Q

Where do naive B cells clonally proliferate upon activation?

A

Germinal centre in stromal cells

75
Q

Why is there a lag period before IgM is produced?

How long is this lag period?

A

7-10 days

Due to time for phagocytosis, transport to LN, activation, proliferating and differentiation of B cells

76
Q

How long does a plasma cell exist?

A

3-4 days (Short-lived)

**Can be long-lived under TFH cell regulation

77
Q

What is the process that selects for the antibody that binds most tightly to the pathogen called?

A

Somatic hypermutation

78
Q

What is the first Ab secreted by plasma cells? Is it high or low affinity?

A

Low-affinity IgM Ab

79
Q

What helps B cells switch from low to high affinity Ab production at the germinal centre?

A

Th cells

80
Q

What Ab receptors do phagocytes have to?

A

Have IgG receptors to Fc region of IgG to deliver opsonised pathogens

*No IgM receptors

81
Q

Do different Ab classes have the same antigen specificity?

A

Yes

82
Q

Other than Ab isotype switch, what other functions do Th cells help B cells to gain? (2)

A
  1. Differentiating into LONG-LIVED plasma cells (Stays in bone marrow to secrete Ab for extended period - e.g. vaccine)
  2. Antigen-specific memory B cells
83
Q

When does IgM and IgG intercept? (IgM fall, IgG rise)

A

2 weeks from antigen exposure

84
Q

What is critical for protection during the lag period before Ab is produced?

A

Innate immune system

85
Q

What site of the antibody binds to the antigenic determinant?

A

Variable binding site

86
Q

What do the heavy chain constant region interact with?

A

Effector molecules such as complement, Fc receptors

87
Q

What does membrane-bound IgM do? What configuration is it?

A

It is a monomer, acting as a BCR

88
Q

What configuration is IgM in plasma and secretory fluids?

Why is it not found in tissue?

A

Soluble pentamer.

Due to its large size

89
Q

What are the functions (3) of IgM?

A
  1. Agglutination - immune complex formation
  2. Complement system activation (classical pathway)
  3. Opsonisation
90
Q

What function does agglutination of Ab-Ag serve? (3)

A
  1. Increases efficacy of elimination by enhancing phagocytosis
  2. Different Ab that recognises different Ag can work together -> easier target
  3. Neutralises viral particles to prevent binding and entry
91
Q

What happens when a specific Ag binds to IgM Ab to undergo complement?

A

Fc region conformation change from planar to staple form -> expose multiple C1 binding sites -> C1 binds to stably to at least 2 Fc sites -> Fc region change conformation to expose more binding sites -> eventually C3 convertase production

92
Q

How many IgM and IgG needed to activate complement (recruit C1)?

A

1 IgM- can bind multiple Ag

Several different IgG - to closely located Ag

93
Q

Why is IgM considered an opsonin even though it cannot bind to phagocytes?

A

More efficient at activating complement due to pentameric structure

94
Q

What is the most abundant Ig?

A

IgG

95
Q

Which Ig has the longest T1/2?

A

IgG

96
Q

What is the configuration of IgG?

How many subclasses are there and how are they differentiated?

A

Monomer.

4 sub-classes with different heavy chain

97
Q

What are the 6 functions of IgG?

A
  1. Agglutination
  2. Complement activation
  3. Foetal immune protection via placental transfer
  4. Neutralisation - aggregate viral particles to prevent entry/ binding
  5. Opsonisation
  6. NK cell activation (Ab-dependent cell-mediated cytotoxicity)
98
Q

How long does the foetus rely on maternal IgG?

What happens when it wanes?

A

Conception to first 6 months after delivery.

May develop Transient Hypogammaglobulinaemia of Infancy (THI) - risk of infection

99
Q

What is the term for the immunity that maternal IgG provides?

A

Passive immunity

100
Q

What kind of bacteria in particular does IgG help to enhance phagocytosis?

A

Encapsulated species such as Gram Negs, S. Aureus and S. pyogenes with hyaluronic acid

101
Q

Which cells have Fcy receptors for IgG?

A

NK cells, Phagocytes

102
Q

What happens when IgG bound to Ag binds to NK cells?

A

Apoptosis of infected cell and pro-inflammatory mediator production

103
Q

What are NK cells activated by?

A

IFNa/B from infected host cells

104
Q

What is the configuration of IgD? What does the membrane-bound form do?
How much of it is found in blood?

A

Monomer.
Serves as BCR to activate B cell.
Extremely low concentration in blood.

105
Q

What is the second most abundant Ig?

How many subtypes are there and what is its configuaration?

A

IgA.
2 subtypes.
Monomeric form in serum for neutralisation and dimeric form in secretory fluids (majority)

106
Q

What is the dimeric IgA connected by?

How is it secreted?

A

J peptide chain

Actively transported across epithelial surface into secretions

107
Q

What roles (2) do dimeric sIgA carry out?

A
  1. Neutralisation at mucosal sites (IgM and IgG cannot be secreted across)
  2. Neonatal immune protection via colostrum and breast milk to protect GIT of neonates
108
Q

What does IgE trigger and what does it protect against?

What is its configuration?

A

Allergic responses.
Against large extracellular parasites.
Monomer.

109
Q

IgE binds to what on what immune cell to cause??

A

binds to FcE receptors on mast cell/ basophils/ eosinophils causing them to degranulate

110
Q

What kind of antigens do TCR recognise?

A

Only peptide antigens presented by MHC molecules

111
Q

Do B cells require MHC peptide antigens to be activated?

A

No, they can respond to non-protein antigen

112
Q

How many unique TCRs does each T cell have? And how many antigens does it respond to?

A

Only 1 copy of unique TCR and each T cell respond to only 1 specific antigen

113
Q

In who are MHC variants the same?

A

IDENTICAL twins

114
Q

What is the difference between MHC Class I and II in terms of expression and presentation?

A

MHC Class I: ALL nucleated cells, presents peptide Ag to CD8+ T cells
MHC Class II: ONLY on APCs (Dendritic cells, macrophages, B cells), presents peptide Ag to CD4+ T cells

115
Q

What stabilises the interaction between TCR and MHC I?

A

CD8 protein

116
Q

What are antigen presenting cells (3)?

A

Dendritic cells, macrophages, B cells

117
Q 
What is the cell that bridges the innate and acquired immune system?
What functions (2) does it have?
A

Dendritic cells.

Phagocytosis and antigen-presentation to T cells

118
Q

What interaction is involved in phagocytosis by dendritic cells?

A

PAMPs and PRRs

119
Q

What effect does TNFa have on dendritic cells?

A

Causes them to mature and increase expression of co-stimulatory molecules on surface

120
Q

Do APCs express MHC I or II?

A

Both

121
Q

What are the 2 signals that are needed for T cells to fully activate (clonal proliferation and differentiation)?

A
  1. Peptide Ag/ MHC complex presentation

2. Co-stimulatory molecules

122
Q

Naive CD4+ T cells become Th0 cells which differentiates into?

A

Effector Th cells

123
Q

What do activated CD4+ T cells secrete and express?

Via what kind of signalling?

A

Secrete T cell growth factor (IL-2) and express IL-2 receptor.
Autocrine-mediated cell proliferation

124
Q

IL-2 is used by which T cells?

A

Used by both antigen-activated CD4+ and CD8+ T cell to proliferate

125
Q

What happens to the reactivated Th1 cell activated by MHC II?

A

Secretes pro-inflammatory cytokines, stimulate ROS production and enhances macrophage mediated intracellular killing (super-activated macrophages)

126
Q

What are 3 microbes that can evade phagolysosomal killing?

A

Listeria, Salmonella, Mycobacteria

127
Q

What happens to effector TFH cells as it move into the B cell zone?

A

Stimulated by MHC II on B cells where TFH cells will stimulate B cells to clonally proliferate and differentiate into long-lived plasma cells and memory cells

128
Q

What do CD8+ T cells differentiate into upon IL-2 stimulation?

A

cytotoxic T lymphocytes

129
Q

How do CTLs kill virally infetced host cells?

A

Specific TCR recognises MHC I viral peptide by infected cell –> releases perforin directly to target cell surface to form a pore, granzymes and granulysin into cell to induce apoptosis
**Minimises bystander damage

130
Q

How do CTLs not react with self?

A

MHC I also displays self-peptides thus CTLs should not react with these cells

131
Q

How long is the T1/2 of T cells?

A

Very long (up to 15 years) - prolonged immunity against viruses

132
Q

When do macrophages switch to its anti-inflammatory role and what does it carry out? (3)

A

After pathogen elimination.

Phagocytose and degrade apoptotic cell debris, secrete anti-inflammatory IL-10 and aid tissue repair

133
Q

What are the 2 primary lymphoid tissues for lymphocyte production and maturation?

A

Red bone marrow and thymus gland

134
Q

Where do lymph not reach? (2)

A

Cartilage and epidermis

135
Q

What helps to transport lymph? (5)

A

valves, breathing, muscle contraction, arterial pulsation, external compression

136
Q

Where are complement proteins produced?

In what state does it exist in circulation?

A

Liver.

Inactive.

137
Q

How long is the T1/2 for cytokines?

A

Short

138
Q

What are the granular cells that defend against large antibody-coated pathogens that cannot be phagocytosed?

A

Mast cell (tissue-resident), Eosinophils, Basophils

139
Q

Where do monocytes differentiate?

A

After migrating into peripheral tissues

140
Q

What do multi-potent haematopoietic stem cells differentiate into? (2)

A 
Lymphoid progenitor (Large/NK cells and small lymphocytes - T/B cells)
Myeloid progenitor

Principles (14 decks)

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