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Phase 2a Lecture Notes > Immunology > Flashcards

Immunology Flashcards

1
Q

Factors affecting immune health

A

Chronic stress, physical inactivity, over exercise, poor personal hygiene, impaired microbiota, environmental toxins, lack of sleep, substance abuse, nutrient deficiencies, poor diet

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2
Q

Examples of autoimmune diseases

A

MS, coeliac’s disease, eczema and psoriasis, asthma, Hashimoto’s thyroid, rheumatoid arthritis

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3
Q

Environmental factors that causes cancer

A

UV, chemicals, pathogens (HPV causes cervical cancer), smoking

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4
Q

Percentages of cancer caused by transformations of germline cells and somatic cells

A

Germline (inheritable) <10%
Somatic (noninheritable) >90%

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5
Q

Cancer immunosurveillance

A

Immune system can recognize and destroy nascent, transformed cells, normal control

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6
Q

Cancer Immunoediting

A

Tumour tend to be genetically unstable, thus immune system can kill and also induce changes in the tumour resulting in tumour escape and recurrence

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7
Q

Tumour specific antigens

A

Are only found on tumours, as a result of point mutation or gene rearrangement, Derive from viral antigens

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8
Q

Tumour Associated Antigens (TAA)

A

-Found on both normal and tumour cells, but are overexpressed on cancer cells
-Developmental antigens which become derepressed. (CEA)
-Differentiation antigens are tissue specific
-Altered modification of a protein could be an antigen

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9
Q

Evidence for human tumour immunity

A

-Spontaneous regression: melanoma, lymphoma
-Regression of metastases after removal of primary tumour: pulmonary metastases from renal carcinoma
-Infiltration of tumours by lymphocytes and macrophages: melanoma and breast cancer
-Lymphocyte proliferation in draining lymph nodes
-Higher incidence of cancer after immunosuppression, immunodeficiency (AIDS, neonates), aging, etc.

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10
Q

Evidence for Escape (detectable tumours)

A

-Immune responses change tumours such that tumours will no longer be seen by the immune system: tumour escape
-Tumours change the immune responses by promoting immune suppressor cells: immune evasion

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11
Q

Examples of Active immunotherapy for cancer treatment

A

Vaccinations ie killed tumour vaccines and purified tumour antigens

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12
Q

Examples of passive immunotherapy for cancer treatment

A

-Adoptive Cellular Therapy (T cells)
-Anti-tumour Antibodies (Her-2/Neu, CD20, CD10, CEA, CA-125, GD3 ganglioside)

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13
Q

How do cell-based cancer therapy work?

A

Cellular therapies can be used to activate a patient’s immune system to attack cancer
They can also be used as delivery vehicle to target therapeutic genes to attack the tumour

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14
Q

Do cell-based cancer therapy act directly on cancer cells?

A

No. They do not act directly on cancer cells. Instead, they work systemically to activate the body’s immune system.

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15
Q

Tumour hypoxia

A

Hypoxic tumour cells adapt to areas of low oxygen. Prominent feature of malignant tumour. Inability of the blood supply to keep up with growing tumour cells

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16
Q

Problem with tumour hypoxia

A

Poor patient prognosis
-Stimulates new vessel growth
-Suppresses immune system
-Resistant to radio- and chemotherapy (repopulate the tumour)
-Increased tumour hypoxia after therapy

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17
Q

Passive Immunisation

A

The administration of pre-formed “immunity” from one person or animal to another person

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18
Q

Passive Immunity Pros and cons

A

Pros-Gives immediate protection effective in immunocompromised patients
Cons-Short-lived possible transfer of pathogens serum sickness” on transfer of animal sera
-Only humoral (antibody) mediated (not work if cell mediated!)

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19
Q

3 main types of vaccines

A

-Using whole bacteria/vaccine
-Parts that trigger the immune system
-Genetic material via a vector

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20
Q

Whole microbe vaccine

A

Bacteria/viruses grown in vitro and inactivated using agents. Don’t cause infection but induce immune response

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21
Q

Limitations of whole microbe vaccine

A
  • The organisms must be grown to high titre in vitro (viruses and some bacteria difficult/expensive to grow in the lab)
  • Whole pathogens can cause excessive reactogenicity (i.e., adverse reactions, excessive immunological responses)
  • Immune responses are not always close to the normal response to infection, e.g., no mucosal immunity, no CD8 Tc responses
  • Usually need at least 2 shots
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22
Q

Live attenuated vaccines

A

The organisms replicate within the host and induce an immune response which is protective against the wild-type organism but does not cause disease

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23
Q

Attenuation

A

Where an organism is cultured in such a way that it does not cause disease when inoculated into humans. Lost its pathogenicity but retains its antigenicity

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24
Q

Pros of attenuated vaccines

A

-Immune response more closely mimics that following real infection because its not fixed – no shape change.
-Better immune response so lower doses are required, so the scale of in vitro growth needed is lower.
-Route of administration may be more favourable (oral).
-Fewer doses may be required to provide protection.

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25
Q

Cons of Live Attenuated Vaccines

A
  • Often impossible to balance attenuation and immunogenicity
  • Reversion to virulence
  • Transmissibility
  • Live vaccines may not be so attenuated in immunocompromised hosts
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26
Q

Why do some pathogens on have vaccines?

A

-Pathogen too difficult to grow
-Killed pathogen not protective (shape change)
-Impossible to obtain attenuated and suitably immunogenic strain
-Too many strains causing disease etc.

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27
Q

Recombinant proteins vs Synthetic peptides

A

Recombinant- Genetically Engineered and produced from bacteria, yeast, insect or mammalian cells.
Synthetic- Peptides synthesized directly using a machine - avoids the need for pathogen growth

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28
Q

Live Attenuated Vectors – Viral Vector

A

These vaccines are composed of living viruses or bacteria that are innocuous to the host but can replicate in host tissues and induce immune responses.
The genes encoding foreign antigens can be inserted into these vectors to produce multivalent vaccines that promise to induce immunity to more than one target disease after the administration of a single dose of vaccine.

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29
Q

DNA vaccines

A

A mammalian plasmid containing DNA that encodes for the foreign protein (yellow) of interest is injected directly.
This requires a lipid nanocarrier to get the DNA into a human cell. The DNA goes to the nucleus, gets transcribed and the foreign protein expressed with MHC to stimulate the immune response

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30
Q

Innate Immunity

A

Instinctive, non-specific, does not depend on lymphocytes, present from birth

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31
Q

Adaptive Immunity

A

Specific ‘Acquired/learned’ immunity, requires lymphocytes, antibodies

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32
Q

Haematopoiesis

A

The commitment and differentiation processes that leads to the formation of all blood cells from pluripotent haematopoietic stem cells

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33
Q

What determines what BC multipotential hematopoietic stem cell differentiates into

A

Colony stimulating factors

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34
Q

Examples of Polymorphonuclear
leukocytes

A

Neutrophil, Eosinophil, basophils

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35
Q

Examples of Mononuclear leukocytes

A

Monocytes (produces macrophages), T-cells, B-cells (produces plasma cells), Mast cells, natural killer cell, dendritic cells (Kupffer in liver, Langerhans in skin)

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36
Q

Soluble factors in the immune system

A

Complement
Antibodies
Cytokines, Chemokines

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37
Q

Complement

A

Group of ~20 serum proteins secreted by the liver that need to be activated to be functional
Modes of action:
1. Direct lysis
2. Attract more Leukocytes to site of infection
3. Coat invading organisms

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38
Q

Antibodies/immunoglobulins

A

Bind to specific antigens
IgG- must abundant
IgM- 10%, primary immune response
IgA- 15%, main antibody in bodily secretions
IgD- 1%, present on B cells
IgE-0.05%, membrane bound on mast cells, involved in histamine response

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39
Q

Structure of antibodies

A

2 Heavy chains and 2 light chains, Fab region found on light chains (site for antigen binding), FC region found on heavy chains ( interacts with cell surface receptors)

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40
Q

Epitope

A

Found on antigen of microbe. Group of amino acids or other chemical groups exposed on the surface of a molecule, frequently a protein, which can generate an antigenic response and bind antibody

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41
Q

Cytokines

A

proteins secreted by immune and non-immune cells, directs immune response

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42
Q

Chemokines

A

Chemotactic cytokines, direct movement of leukocytes (and other cells) from the bloodstream into the tissues or lymph organs by binding to specific receptors on cells, little magnets in body drawing WBC to infection

43
Q

Inflammatory response to tissue damage or infection

A

-Stop bleeding (coagulation)
-Acute inflammation (leukocyte recruitment)
-Kill pathogens, neutralise toxins, limit pathogen spread
-Clear pathogens/dead cells (phagocytosis)
-Proliferation of cells to repair damage
-Remove blood clot – remodel extracellular matrix
-Re-establish normal structure/function of tissue

44
Q

Inflammation

A

A series of reactions that brings cells and molecules of the immune system to sites of infection or damage

45
Q

Acute inflammation

A

Complete elimination of a pathogen followed by resolution of damage, disappearance of leukocytes and full regeneration of tissue

46
Q

Chronic inflammation

A

Persistent, un-resolved inflammation, typically something wrong with immune system

47
Q

Cells responsible for sensing microbes

A

In blood – Monocytes, Neutrophils
In tissues – Macrophages, Dendritic cells

48
Q

PRR- Pattern Recognition Receptors

A

Detect PAMP ( Pathogen-Associated Molecular Patterns) found on microbes

49
Q

Examples of PRR- Pattern Recognition Receptors

A

Lectin Receptors- bind to foreign carbohydrates on viruses or microbes
Scavenger Receptors- bind to foreign lipids on viruses or microbes
Tool-like Receptors- different toll-like receptors bind to different foreign molecules on viruses or microbes

50
Q

Complement activation pathways

A

Classical - Ab bound to microbe, antigen-antibody complexes
Alternative – C’ binds to microbe
Lectin – activated by mannose
binding lectin bound to microbe

51
Q

Functions of Complement

A

Lyse microbes directly (MAC)
Chemotaxis- phagocytises
Opsonisation- to tag foreign pathogens for elimination by phagocytes

52
Q

Extravasation (Diapedesis)

A

process in which white blood cells come out of the intact blood vessels into the surrounding area in case of injury
Rolling/tethering, 2nd adhesion, spreading, transmigration

53
Q

Stages of phagocytosis

A
  1. Binding
  2. engulfment
  3. phagosome formation-acidification cytotoxic molecules proteolysis
    4.phagolysosome- cytoplasmic body formed by the fusion of a phagosome with a lysosome
    5.membrane disruption/fusion- secretion and antigen presentation
54
Q

Mechanisms of Microbial Killing
O2-dependent

A

-Superoxides (O2-) are converted to H2O2 then ·OH (free radical)
-Nitric Oxide (NO) – vasodilation (Viagra) increase extravasation but also anti-microbial

55
Q

Mechanisms of Microbial Killing
O2-independent

A

Enzymes: (eg lysozyme)
Proteins: defensins (insert into membranes), TNF
pH

56
Q

Why do we need Adaptive Immunity?

A

Microbes evade innate immunity (proteases, decoy proteins, etc)
Intracellular viruses and bacteria ‘hide’ from innate immunity
Need memory to specific antigen – ‘seen it before so faster response’

57
Q

Cell-Mediated Immunity

A

Interlay between Antigen Presenting Cells (APC)
(Macrophages, Dendritic Cell, B cells) and T cells.
Requires intimate cell to cell contact
– to control Ab responses via contact with B cells
– to directly recognise and kill viral infected cells
To recognise self or non-self

58
Q

T cell selection

A

T cells that recognise self are killed in the foetal thymus as they mature, adult T cells only recognise non self

59
Q

T cell recognition of antigen

A

MHC (major histocompatibility complex) molecule of infected cell presents peptide, Antigen peptide bound to MHC molecule, T cell receptor recognizes MHC and peptide

60
Q

MHC class 1

A

All cells except RBC, intrinsic (intercellular ie viral infection), function-kill infected cell with intracellular pathogen

61
Q

MHC class 2

A

APC (antigen presenting cells) only, extrinsic (extracellular ie phagocytosis), Help B cells make Ab to extracellular pathogen, can help directly kill

62
Q

Naïve T cells

A

Not been activated yet, ie not bound yet

63
Q

TH2 cell

A

antibody production

64
Q

TH1 cell

A

Helps Kill Intracellular pathogens

65
Q

CD8 T cell activation

A

CD8 + MHCI/peptide = Tc / CTL
CTL forms proteolytic granules &
releases perforins and granulysin
Also induces apoptosis (cell suicide)

66
Q

Th1 (CD4) Activation

A

APC presents Ag with MHC II to a naïve CD4 T cell
Stimulation with high levels of IL-12 activate naïve cells to CD4 Th1 cells
Th1 cells travel to secondary lymphoid tissue (spleen, lymph nodes)
Activated CD4 Th1 cells proliferate (clonal expansion)
Th1 cell recognises Ag on infected cells (with MHC II) via TCR (CD4)
Th1 secretes INFγ – stop virus spread (apoptosis)

67
Q

B cell activation

A

B cells express membrane bound Ig (IgM or IgD monomer)
Each B cell can only make one Ab that will only bind one epitope on one Antigen
B cells that recognise self are killed in bone marrow

68
Q

How T cells help B cells- Clonal expansion

A

APC eats Ag (extrinsic) and presents it to naïve CD4+ T cells (via MHC II)

These turn into primed Th2 cells

Th2 cells bind to B cells that are presenting same Ag (via MHC II). This Ag has been captured using the mIgR on cell surface.

Th2 cell now secretes cytokines

These cause B cells to divide – CLONAL EXPANSION and differentiate into:

Plasma cells (AFC = antibody forming cell) and
Memory B cells (Bm)

69
Q

Examples of PAMPS (Pathogen associated molecular patterns)

A

Bacteria- Lipoteichoic acid (LTA), peptidoglycan (PGN), lipoproteins, DNA, flagellin, lipopolysaccharide (LPS)
Viruses- Coat protein, nucleic acid

70
Q

Why does the immune system recognise patterns?

A

To vastly expand the repertoire of ligands they can bind
Traditional lock and key model- Antigen and antibody
Master key- PRRS

71
Q

Damage associated molecular patterns (DAMPs)

A

Endogenous molecules created to alert the host to tissue injury and initiate repair.

72
Q

Why don’t these intracellular molecules activate PRRs normally (in health)?

A

Our DNA and RNA is normally located within the nucleus or mitochondria where PRRs (pattern recognition receptors) cannot access it

73
Q

TLR (toll-like receptors) signalling- PAMPs

A

Different TLRs activate different signalling cascades depending on the pathogen being detected to tailor the immune response that is generated

74
Q

RIG-I-like Receptors (RLRs)

A

detect viral RNA in the cytoplasm

75
Q

NOD-like Receptors (NLRs)

A

-sensing cytoplasmic bacterial pathogens and DAMPS
-regulation of inflammatory & cell death responses

76
Q

NOD1 and 2

A

Activated by recognition of specific motifs (mostly muropeptides) present in bacterial peptidoglycan (PG)
Dynamically traffic to intracellular membranes upon detection of PG derivatives

77
Q

Why don’t NLRs activate interferons?

A

NLRs detect predominantly intercellular bacteria, Interferons are anti-viral cytokines

78
Q

The “damage chain reaction”

A

High levels of DAMPs are associated with many inflammatory and autoimmune diseases as well as atherosclerosis and cancer.

79
Q

Cytokine storm

A

-Profound increase in cytokines, chemokines & interferons
-Causes severe inflammation and tissue damage
-Induction due to:
-genetic makeup of the host
-persistence of the pathogen (evasion
mechanisms)
Role in sepsis, influenza, severe COVID-19 pathogenesis, etc.

80
Q

Sepsis

A

-Unable to mount a robust but regulated immune response
-Pathogen isn’t cleared = severe infection and dissemination to the circulation (bacteremia,viremia, or fungemia)

81
Q

Who is more likely to develop sepsis

A

More likely in people with immature (neonates and young children) or dysfunctional (old age, immunocompromised) immune response

82
Q

Type I hypersensitivity

A

Immediate reaction to environmental antigens mediated via IgE

83
Q

Atopy

A

inherited trait for Type I hypersensitivity

84
Q

Allergens

A

antigens that trigger allergic reactions

85
Q

First stage of type 1 hypersensitivity reaction

A
  1. Body exposed to allergen
  2. Antigen presenting cells absorb allergen and present it on the MCH2
  3. Naïve T cells attach to MCH2 activating the T cell into a Th2 cell with a antibody for antigen from allergen
  4. Binds to B cell with same antibodies leading to more B cells with specific IgE being produced
  5. IgE binds to mast cell and is present on cell surface. It is primed for next encounter with antigen
86
Q

IgG vs IgE

A

IgG has hinge region, IgE does not. IgE has a much shorter lifespan. IgE is not relevant for bacterial infection.

87
Q

Second encounter with allergen

A
  1. Allergen binds to IgE present on mast cell surface
  2. Trigger cytokine action that causes mast cell degranulation
  3. Degranulation results in the release of inflammatory mediators (ie histamine, prostaglandins, ect) via exocytosis.
88
Q

Effect of Histamine

A

Vasodilatation, increased capillary permeability, chemokinesis, bronchoconstriction

89
Q

Effects of Neutral proteases (tryptases, chymases, carboxypeptidase A)

A

Increased vascular permeability, airway hyperresponsiveness, cell recruitment

90
Q

Allergy symptoms

A

Trouble breathing, itching, sneezing, runny nose, headache, red/watery eyes, hives/rash

91
Q

Late phase response

A

Late reactions can occur without repeated exposure, this is a result of further recruitment of cells at the site of exposure

92
Q

What are the conditions that elicit a type I hypersensitivity reaction?

A

Allergen characteristics
Host factors
Environmental influences

93
Q

What makes certain proteins allergenic?

A

Allergens have the ability to induce a strong IgE response
 Protease activity – Der p 1
 Surface features of protein –Ves v 5
 Glycosylation pattern of protein –Ara h 1

94
Q

Diseases associated with ageing

A

CVD, cancers, autoimmune disease, neurodegenerative disease, covid-19

95
Q

Systematic hallmarks of aging

A

Nutritional dysregulation

96
Q

Cellular level hallmarks of aging

A

Cellular senescence ( eventually stop multiplying but don’t die off when they should), stem cell exhaustion, altered intercellular communication

97
Q

Molecular level hallmarks of aging

A

Genomic instability, telomere shortening, epigenetic alteration, loss of proteostasis, compromised autophagy, mitochondrial dysfunction

98
Q

Immunosenescence

A

the state of dysregulated immune function that contributes to the increased susceptibility of the elderly to infection and possibly to autoimmune disease and cancer

99
Q

myeloid-derived suppressor cells (MDSC)

A

immature myeloid cells with the ability to downregulate adaptative immune responses

100
Q

Efferocytosis

A

the effective clearance of apoptotic cells by phagocytes

101
Q

Senescence-associated secretory phenotype (SASP)

A

phenotype associated with senescent cells wherein those cells secrete high levels of inflammatory cytokines, immune modulators, growth factors, and proteases

102
Q

Factors that can cause Senescence

A

Telomere erosion, oncogene (mutated gene that has the potential to cause cancer) activation, DNA damage, oxidative stress, irradiation, chemotherapy, iPSC reprogramming, developmental cues, tissue damage

103
Q
A

Phase 2a Lecture Notes (14 decks)

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