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Pase 2a Notes > Immunology > Flashcards

Immunology Flashcards

1
Q

9 factors that affect immune health

A

Lack of sleep
Substance use e.g. alcohol
Poor diet
Nutrient deficiencies
Chronic stress environmental toxins
Impaired microbes
Poor personal hygiene
Physical inactivity

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2
Q

4 types of immunotherapies

A

Monoclonal antibodies
Cytokines
Vaccines
Cell therapy

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3
Q

Hallmarks of cancer

A

Grow self-sufficiently
Evades apoptosis
Ignores anti-proliferation signals
Limitless replication potential
Sustained angiogenesis
Invades tissues
Escapes immune surveillance

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4
Q

Tumour immunology goal

A

Clinically induced anti-tumour immune response which discriminates tumour and non tumour cells

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5
Q

Cancer immuno surveillance vs immunoediting

A

S - immune recognises and destroy nascent transformed cells

I - immune kills or induce changes in tumour escape and recurrance

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6
Q

Tumour Specific vs Associated antigens

A

S - only found on tumours due to point mutation

A - found on normal but over expressed on tumour cells and tissue specific

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7
Q

Evidence for human tumour immunity

A

Spontaneous regression
Infiltration of tumour by lymphocytes and macrophages
Higher incidence of cancer after immunosuppressant

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8
Q

Active vs passive immunotherapy

A

Passive activates the immune system rather than attacking the tumour

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9
Q

2 functions of cell based therapy

A

To activate immune system

As a delivery vechile or target therapeutic genes to attack the tumour’

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10
Q

How to make a DC vaccine

A

Dendritic Langerhan cells of epidermis detect and chew up foreign proteins then present a piece on the surface. Blood of the cancer patient is collected and enriched to increase population of dendritic cells

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11
Q

6 active immunotherapy vaccines

A

Killed tumour
Purified tumour antigens
Professional APC-based
Cytokine enhanced
DNA
Viral vectors

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12
Q

2 passive immunotherapies

A

Adoptive cellular therapy (T Cells)
Anti-tumour antibodies

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13
Q

What is a prominent feature of malingnant tumours?

A

Hypoxia (tumour cells have adapted to low oxygen)

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14
Q

Why is hypoxia in tumours a problem?

A

Stimulates new vessel growth, suppresses immune system, resistant to radio and chemotherapy so poor patient prognosis

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15
Q

3 types of traditional vaccines

A

Whole
Live attenuated
Toxoids

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16
Q

Define passive immunity

A

Short term from a introduction of antibodies from another person or animal

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17
Q

Adv and Dis of passive immunity

A

A - immediate protection and effective in immunocompromised

D - short lived, possible transfer of pathogens and only humourly mediated

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18
Q

2 types of specific immunoglobulin

A

Human normal- pooled from donors

Convalescing serum e.g. Covid

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19
Q

Define active immunity

A

Non living, toxoids or live attenuated agents or materials to trigger a response

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20
Q

Limits of non living vaccines

A

Adv - Does not cause an infection

Dis - organism must be grown in vitro and needs at least 2 vaccines
Causes excessive reactions

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21
Q

What are toxoids?

A

Inactivated toxins = non living vaccines

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22
Q

Adv and Disv of live attenuated vaccines

A

Adv - Immune response closely mimic real infection, route of administration is favourable, fewer and lower doses means in vitro growth is less

Dis - transmissibility, reversion to virulence, impossible to balance attenuation and immunogenicity so hard in immunocompromised

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23
Q

Why are so many pathogens lacking vaccines? E.g. HIV, malaria, herpes

A

Pathogen is hard to grow and impossible to obtain attenuated and immunogenicity strain. Killed pathogen is not affective and too many strains causing disease

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24
Q

6 novel approaches to vaccines

A

Recombinant proteins. - genetically engineered and produced by bacteria, yeast insect, or mammalian cells
Synthetic peptides - synthesised via machine
Live attenuated vectors. - safe viruses have inserted genes encoding foreign antigens
DNA - mammalian plasmid containing DNA encoding for foreign protein
mRNA - synthesised in vitro
T-independent antigens - bacterial polysaccharides presented on MHC class 2

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25
Q

5 Stages of vaccination

A

Engage innate immune system
Triggers PAMP
Engage TLR receptors
Activate specialist APC
Engage adaptive immune system

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26
Q

Innate vs adaptive immunity

A

Innate - non-specific
Adaptive - specific requires lymphocytes

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27
Q

What stem cell does every blood cell originate from?

A

Haematopoeitic pluripotent stem cell

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28
Q

Blood sample centrifuge forms 3 layers:

A

Upper fluid plasma - water, proteins, sugars, lipids, electrolytes
Middle white - Leukocytes
Lower 45% - erythrocytes, platelets

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29
Q

3 polymorphonuclear leukocytes

A

Neutrophils - 3 nuclear lobes, short lived and innate phagocytosis

Eosiniphils - Induces histamine release in parasitic and allergic reactions

Basophils - interconnecting nuclei release histamines

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30
Q

3 mononuclear leukocytes

A

Monocytes - kidney nucleus differentiates into macrophages

T-cells - Big nucleus

B-cells - differentiates into plasma cells and releases antibodies

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31
Q

3 other immune cells

A

Mast - releases histamine in allergy

Natural Killer - kill tumour and virus by apoptosis

Dendritic - surveillance cells e.g. kupffer

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32
Q

4 soluble factors

A

Complement
Antibodies
Cytokines
Chemokines

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33
Q

Describe complement factors

A

~20 serum proteins secreted by liver and need to be activated by 3 pathway:
Alternative - C binds to microbe
Classical - Ab binds to mcirobe
Lectin - mannose binds to microbe

= Direct lysis, attracts leukocytes and coast invading organisms

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34
Q

Describe antibodies / immunoglobulins

A

Glycoproteins bind to antigens
IgG - crosses placenta
IgA - in breast milk
IgM - primary response
IgE - triggers histamine release
IgD - memory B cells

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35
Q

What is the part of antigen that binds to antibody?

A

Epitope

36
Q

What are the 4 cytokines?

A

Proteins secreted by immune and non-immune cells for communication:

Interferons - induce antiviral resistance
Interleukins - cause cell division and differentiation
Colony Stimulating Factors - directs division and differentiation
Tumour necrosis factors - mediates inflammation, apoptosis and cytotoxic

37
Q

Describe chemokines

A

40 proteins attract leukocytes to sites of inflammation by binding to specific receptors

38
Q

Innate vs adaptive immunity

A

I - primitive instinct 1st line of defence
Slow with no long memory

A - quicker response and memory to specific antigen

39
Q

Innate immunity is composed of 3

A

Physical and chemical barriers (skin, mucus)
Phagocytosis cells (neutrophils, macrophages)
Serum proteins (complement)

40
Q

3 hallmarks of inflammatory response

A

Increased blood supply
Increased vascular permeability
Increased leukocytes extravastion

41
Q

Steps of an inflammatory response

A

Coagulation to stop bleeding
Acute inflammation leukocytes recruit
Kill pathogens, neutralise toxins
Phagocytise dead pathogens and cells
Proliferation to repair damage
Remove blood clot
Reestablish normal structure

42
Q

Acute vs chronic inflammation

A

A - complete elimination of pathogen followed by resolution of damage

C - persistent, un-resolved inflammation

43
Q

What happens in an innate response (4 steps)

A
  1. Sense microbes by binding ( PRR / PAMP)
  2. Rolling (neutrophils bind to antigens on endothelium and slow down)
  3. Extravasation ( increased vascular permeability forms oedema)
  4. Phagocytosis
44
Q

2 mechanisms of microbial killing

A

O2 dependent - Reactive Pxygen Intermediates release free radicals / NO

O2 independent - enzymes and proteins

45
Q

What display peptides differentiate self from non-self proteins?

A

Major histocompatibolity complex (MHC)

46
Q

3 MHCs

A

1 - glycoproteins on all nucleated cells
2 - glycoprotein only on APC
3 - code for secreted proteins

47
Q

Intrinsic vs extrinsic pathways use which MHCs?

A

Intrinsic - class 1 MHC, Tc (CD8) kills infected cell with Intracellular pathogen

Extrinsic - class 11 MHC, Th (CD4) helps B cells make Ab to Extracellular pathogen

48
Q

Why do we need adaptive immunity?

A

Microbes evade or hide from innate immunity
Need memory to specific antigens

49
Q

What do cell mediated immunity require for recognition?

A

Intimate cell to cell contact
Major histocompatibility complex
Intrinsic antigens
Extrinsic antigens

50
Q

Do t lymphocytes respond to soluble antigens?

A

No!
Only Intracellular presented antigens

51
Q

Naive cells can be activated when:

A

High interleukin 12 - CD4 secretions help TH1 (CD4) and Tc (CD8) phagocytoses

Low interleukin 12 - CD4 secretions help TH2 antibody production

52
Q

3 functions of antibodies

A

Neutralise toxins by binding
Increase opsonisation - phagocytosis
Activate compliment

53
Q

What does the innate immune use to recognise pathogens?

A

Molecular patterns - highly conserved and expressed by a large group of pathogens

54
Q

Problems with innate immunity

A

Takes a long time
Not highly specific
Lots of bacterial species and viruses

55
Q

What do innate immunity recognise on pathogens but not on host cells

A

Pathogen Associated Molecular Patterns (PAMP)

Damage Associated Molecular Patterns (DAMP)

Can be secreted or cell-associated e.g. peptidoglycans, liposaccharides, nuclei acids

56
Q

Why recognise patterns instead of traditional lock and key shape?

A

Allows for flexibility so expands repertoire of ligands they can bind to

57
Q

What do innate immunity recognise when tissue injury occurs?

A

Damage Associated Molecular Patterns (DAMP)

Endogenous molecules created to alert and initiate repair e.g. DNA, RNA, ATP, uric acid, mutations, UVB

58
Q

What are the 2 types of PRRs?

A

Pattern Recognition Receptors:

Secreted and circulating
- Antimicrobial peptides secreted into lining fluid
- Lectins and collections activate complement and phagocytosis

Cell associated
- Receptors on cell membrane or cytosol, mostly Toll-like receptors signalling cascades

59
Q

How are pathogens that are not Extracellular dealt with? E.g. virus/ bacteria

A
  1. RIGI-Like receptors (RGR) detect viral RNA in cytoplasm
  2. NOD-Like receptors (NLR) sense cytoplasmic bacteria and DAMPs
60
Q

Describe a damage chain reaction

A

Harmful stimuli cause tissue damage and release of DAMPs
TLRs are activated and release pro-inflammatory mediators
Inflammation recruits more DAMPs

61
Q

Describe steps of a cytokine storm

A

Increase I cytokines, chemokines and interferons causes severe inflammation and tissue damage.
Infection or persistence causes sepsis etc

62
Q

2 main immunomodulation strategies

A

Agonists enhance TLR signalling
- promotes protective responses
- potentially enhances inflammation
Antagonists inhibit TLR signalling
- blocks binding
- potentially allows pathogen outgrowth or mutation

63
Q

Define allergy

A

Type 1 hypersensitivity is an immediate reaction to allergens mediated via IgE

64
Q

What is Atopy?

A

Inherited trait to develop exaggerated reactions for type 1 hypersensitivity

65
Q

Describe immunoglobulin E structure

A

2 heavy and 2 light chains with a constant range to dictate IgE and variable sites due to gene splicing

66
Q

Steps of a type 1 hypersensitivity

A
  1. Sensitisation - fine tuning to recognise harmful allergens
  2. Mast cell degranulation - factory of pro inflammatory cytokines and exocytosis
  3. Early phase mediators - histamine, tryptase, chymotryptin etc
67
Q

What happens in sensitisation?

A

Allergens pass through physical barrier, taken up by APC and presented to naive T cells.Th32 cells activate B cells to release immunoglobulins which bind to mast cells

68
Q

What happens when mast cells degranulate?

A

Cross linking of receptors leads to influx of calcium and activation of transcription factors. Use of aleuronic acid from cell membrane to produce cytokines and mediators

69
Q

2 types of IgE receptors

A

High affinity (FCR1) - main instigator
- Eosinophils, basophils, mast cells
Low affinity (FCR11) - more widely distributed
- B, T cells, monocytes, platelets, neutrophils

70
Q

Why is there a late phase response?

A

Recruitment of other cells to site prolongs inflammatory response

71
Q

What 3 conditions are required for type 1 hypersensitivity?

A
  1. Protein allergen characteristics - protease activity, surface features and glycosylation pattern
  2. Host factors - genes
  3. Environmental influences - diminished encounter of microbes
72
Q

What is a pseudo-type 1 reactions?

A

Not IgE mediated but leads to mast cell degranulation
E.g. allergic rhinitis, venom allergy, anaphylaxis

73
Q

Anaphylaxis treatments

A

Adrenaline / epinephrine
Antihistamines
Corticosteroids
Bronchodilation
Fluid resuscitation
Desensitisation

74
Q

Is asthma type 1?

A

Nope
It’s complex - partially type 1, 4, 5

75
Q

Allergy clinical indications

A

Anaphylaxis
Airway constriction
Excessive mucus production
Abdominal bloating, vomiting, diarrhoea
Epithelial - eczema, itching, red

76
Q

Cells involved with IgE

A

Mast, Eosiniphils, lymphocytes, dendritic
Smooth muscle, fibroblasts, epithelia

77
Q

10 hallmarks of ageing

A

Systemic level
- Nutritional dysregulayion
Cellular level
- cellular senescence
- stem cell exhaustion
Altered intercellular communication
Molecular level
- geonomic instability
- telomere shortening
- epigenetic alteration
- loss of proteostasis
- compromised autophagy
- mitochondrial dysfunction

78
Q

Hat happens during immunosenescence

A

Innate response
Adaptive response
Inflammation - excess inflammation
Reduced antigen presentation
Reduced chemotaxis
= increased susceptibility to infection, cancer etc

79
Q

What is macrophage efferocytosis?

A

Killing debris and neutrophils, release of pro-resolution cytokines
(Impaired with ageing)

80
Q

How are neutrophils, monocytes, and cells and dendritic cells altered with age?

A

can’t produce molecules for killing or trapping so can’t chemotaxis or phagocytosis

81
Q

What is called when cells lose the ability to divide and differentiate?

A

Senescence-Associated Secretory Phenotype (SASP)

82
Q

What happens during senescence?

A

Tissue damage
Cell cycle arrest enlarges cell size
Large production of molecules not seen in normal cells

83
Q

Factors to look for in senescence

A

Primitive organisation
Cell cycle at rest
Alterations in metabolic reaction
Lysosomes
Chemokines
Reduction of cytokines and MMPs

84
Q

What happens in REDOX imbalance

A

Pro and anti-inflammatory molecules are imbalanced causing oxidative stress and ROS damage tissues

Proteases also increase so emphysemas increase

85
Q

Immune response changes with immunosenescence

A

Reduced naive B and T cells
Increased B and T cells
Increased senescence cells
Reduced antibody production

Pase 2a Notes (6 decks)

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