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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
5 Stages of vaccination
Engage innate immune system Triggers PAMP Engage TLR receptors Activate specialist APC Engage adaptive immune system
26
Innate vs adaptive immunity
Innate - non-specific Adaptive - specific requires lymphocytes
27
What stem cell does every blood cell originate from?
Haematopoeitic pluripotent stem cell
28
Blood sample centrifuge forms 3 layers:
Upper fluid plasma - water, proteins, sugars, lipids, electrolytes Middle white - Leukocytes Lower 45% - erythrocytes, platelets
29
3 polymorphonuclear leukocytes
Neutrophils - 3 nuclear lobes, short lived and innate phagocytosis Eosiniphils - Induces histamine release in parasitic and allergic reactions Basophils - interconnecting nuclei release histamines
30
3 mononuclear leukocytes
Monocytes - kidney nucleus differentiates into macrophages T-cells - Big nucleus B-cells - differentiates into plasma cells and releases antibodies
31
3 other immune cells
Mast - releases histamine in allergy Natural Killer - kill tumour and virus by apoptosis Dendritic - surveillance cells e.g. kupffer
32
4 soluble factors
Complement Antibodies Cytokines Chemokines
33
Describe complement factors
~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
34
Describe antibodies / immunoglobulins
Glycoproteins bind to antigens IgG - crosses placenta IgA - in breast milk IgM - primary response IgE - triggers histamine release IgD - memory B cells
35
What is the part of antigen that binds to antibody?
Epitope
36
What are the 4 cytokines?
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
Describe chemokines
40 proteins attract leukocytes to sites of inflammation by binding to specific receptors
38
Innate vs adaptive immunity
I - primitive instinct 1st line of defence Slow with no long memory A - quicker response and memory to specific antigen
39
Innate immunity is composed of 3
Physical and chemical barriers (skin, mucus) Phagocytosis cells (neutrophils, macrophages) Serum proteins (complement)
40
3 hallmarks of inflammatory response
Increased blood supply Increased vascular permeability Increased leukocytes extravastion
41
Steps of an inflammatory response
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
Acute vs chronic inflammation
A - complete elimination of pathogen followed by resolution of damage C - persistent, un-resolved inflammation
43
What happens in an innate response (4 steps)
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
2 mechanisms of microbial killing
O2 dependent - Reactive Pxygen Intermediates release free radicals / NO O2 independent - enzymes and proteins
45
What display peptides differentiate self from non-self proteins?
Major histocompatibolity complex (MHC)
46
3 MHCs
1 - glycoproteins on all nucleated cells 2 - glycoprotein only on APC 3 - code for secreted proteins
47
Intrinsic vs extrinsic pathways use which MHCs?
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
Why do we need adaptive immunity?
Microbes evade or hide from innate immunity Need memory to specific antigens
49
What do cell mediated immunity require for recognition?
Intimate cell to cell contact Major histocompatibility complex Intrinsic antigens Extrinsic antigens
50
Do t lymphocytes respond to soluble antigens?
No! Only Intracellular presented antigens
51
Naive cells can be activated when:
High interleukin 12 - CD4 secretions help TH1 (CD4) and Tc (CD8) phagocytoses Low interleukin 12 - CD4 secretions help TH2 antibody production
52
3 functions of antibodies
Neutralise toxins by binding Increase opsonisation - phagocytosis Activate compliment
53
What does the innate immune use to recognise pathogens?
Molecular patterns - highly conserved and expressed by a large group of pathogens
54
Problems with innate immunity
Takes a long time Not highly specific Lots of bacterial species and viruses
55
What do innate immunity recognise on pathogens but not on host cells
Pathogen Associated Molecular Patterns (PAMP) Damage Associated Molecular Patterns (DAMP) Can be secreted or cell-associated e.g. peptidoglycans, liposaccharides, nuclei acids
56
Why recognise patterns instead of traditional lock and key shape?
Allows for flexibility so expands repertoire of ligands they can bind to
57
What do innate immunity recognise when tissue injury occurs?
Damage Associated Molecular Patterns (DAMP) Endogenous molecules created to alert and initiate repair e.g. DNA, RNA, ATP, uric acid, mutations, UVB
58
What are the 2 types of PRRs?
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
How are pathogens that are not Extracellular dealt with? E.g. virus/ bacteria
1. RIGI-Like receptors (RGR) detect viral RNA in cytoplasm 2. NOD-Like receptors (NLR) sense cytoplasmic bacteria and DAMPs
60
Describe a damage chain reaction
Harmful stimuli cause tissue damage and release of DAMPs TLRs are activated and release pro-inflammatory mediators Inflammation recruits more DAMPs
61
Describe steps of a cytokine storm
Increase I cytokines, chemokines and interferons causes severe inflammation and tissue damage. Infection or persistence causes sepsis etc
62
2 main immunomodulation strategies
Agonists enhance TLR signalling - promotes protective responses - potentially enhances inflammation Antagonists inhibit TLR signalling - blocks binding - potentially allows pathogen outgrowth or mutation
63
Define allergy
Type 1 hypersensitivity is an immediate reaction to allergens mediated via IgE
64
What is Atopy?
Inherited trait to develop exaggerated reactions for type 1 hypersensitivity
65
Describe immunoglobulin E structure
2 heavy and 2 light chains with a constant range to dictate IgE and variable sites due to gene splicing
66
Steps of a type 1 hypersensitivity
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
What happens in sensitisation?
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
What happens when mast cells degranulate?
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
2 types of IgE receptors
High affinity (FCR1) - main instigator - Eosinophils, basophils, mast cells Low affinity (FCR11) - more widely distributed - B, T cells, monocytes, platelets, neutrophils
70
Why is there a late phase response?
Recruitment of other cells to site prolongs inflammatory response
71
What 3 conditions are required for type 1 hypersensitivity?
1. Protein allergen characteristics - protease activity, surface features and glycosylation pattern 2. Host factors - genes 3. Environmental influences - diminished encounter of microbes
72
What is a pseudo-type 1 reactions?
Not IgE mediated but leads to mast cell degranulation E.g. allergic rhinitis, venom allergy, anaphylaxis
73
Anaphylaxis treatments
Adrenaline / epinephrine Antihistamines Corticosteroids Bronchodilation Fluid resuscitation Desensitisation
74
Is asthma type 1?
Nope It’s complex - partially type 1, 4, 5
75
Allergy clinical indications
Anaphylaxis Airway constriction Excessive mucus production Abdominal bloating, vomiting, diarrhoea Epithelial - eczema, itching, red
76
Cells involved with IgE
Mast, Eosiniphils, lymphocytes, dendritic Smooth muscle, fibroblasts, epithelia
77
10 hallmarks of ageing
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
Hat happens during immunosenescence
Innate response Adaptive response Inflammation - excess inflammation Reduced antigen presentation Reduced chemotaxis = increased susceptibility to infection, cancer etc
79
What is macrophage efferocytosis?
Killing debris and neutrophils, release of pro-resolution cytokines (Impaired with ageing)
80
How are neutrophils, monocytes, and cells and dendritic cells altered with age?
can’t produce molecules for killing or trapping so can’t chemotaxis or phagocytosis
81
What is called when cells lose the ability to divide and differentiate?
Senescence-Associated Secretory Phenotype (SASP)
82
What happens during senescence?
Tissue damage Cell cycle arrest enlarges cell size Large production of molecules not seen in normal cells
83
Factors to look for in senescence
Primitive organisation Cell cycle at rest Alterations in metabolic reaction Lysosomes Chemokines Reduction of cytokines and MMPs
84
What happens in REDOX imbalance
Pro and anti-inflammatory molecules are imbalanced causing oxidative stress and ROS damage tissues Proteases also increase so emphysemas increase
85
Immune response changes with immunosenescence
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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