Immunology Flashcards

1
Q

Define Innate immunity

A
  • Non-specific
  • 1st line of defence
  • Provides barrier to antigen
  • Is present from birth
  • No long lasting memory
  • Does not require lymphocytes
  • Fast
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2
Q

Define Adaptive immunity

A
  • Specific
  • ‘Acquired’ immunity
  • Response specific to antigen
  • Memory to specific antigen
  • Quicker response
  • Requires lymphocytes
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3
Q

What is a Haematopoietic pluripotent stem cell (haemocytoblast)

A

The stem cell that every blood cell in the body originates from

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4
Q

Give examples of polymorphonuclear leukocytes

A
  • They have more than one nucleus

- e.g. Neutrophils, eosinophils and basophils

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5
Q

Give examples of mononuclear leukocytes

A
  • They have one nucleus

- e.g. Monocytes (kidney shaped nuclei), T-cells and B-cells (lymphocytes)

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6
Q

What cells are involved in the immune system?

A
  • Neutrophils
  • Monocytes
  • Macrophages
  • Eosinophil
  • Basophil
  • Mast cell
  • T Lymphocytes (T cells)
  • B Lymphocytes ( B cells)
  • Natural killer cells
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7
Q

What role do Neutrophils play in the immune system?

A
  • Plays an important role in innate immunity (phagocytosis)
  • 2 main intracellular granules
  • Primary lysosomes – can kill microbes by secreting toxic substances
  • Secondary granules
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8
Q

What role do Monocytes play in the immune system?

A
  • Plays an important role in innate AND adaptive immunity (phagocytosis and antigen presentation)
  • Differentiate into macrophages in the tissues
  • Main role – remove anything foreign (microbes) or dead
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9
Q

What role do macrophages play in the immune system?

A
  • Innate and adaptive (phagocytosis + antigen presentation)
  • Reside in tissues, lifespan – months/years e.g. Kupffer cells – liver, microglia – brain
  • Most often first line of non-self recognition
  • Main role – remove foreign (microbes) and self (dead/tumour cells)
  • Present Antigen to T-cells
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10
Q

What role do Eosinophils play in the immune system?

A
  • Eosinophils are mainly associated with parasitic infections and allergic reactions
  • Lifespan 8-12 days
  • Granules stain for acidic dyes (eosin)
  • Activates neutrophils, induces histamine release from mast cells and provokes bronchospasm
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11
Q

What role do Basophils play in the immune system?

A
  • Mainly involved in immunity to parasitic infections and allergic reactions
  • Lifespan 2 days
  • Granules stain for basic dyes
  • Very similar to mast cells
  • Binding of IgE to receptor causes de-granulation releasing histamine – main cause of allergic reactions
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12
Q

What role do Mast cells ​play in the immune system?

A
  • Only in tissues (precursor in blood)
  • Very similar to basophils
  • Binding to IgE to receptor causes de-granulation releasing histamine – main cause of allergic reactions
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13
Q

What role do T Lymphocytes (T cells) play in the immune system?

A
  • Play major role in adaptive immunity
  • Lifespan hours-years
  • Mature in thymus
  • Found in blood, lymph nodes and spleen
  • Recognise antigen presenting cells (APC)
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14
Q

What are the 4 main types of T cells?

A

1) T helper 1
- Cell-mediated immunity
- Regulate monocytes and macrophages.

2) T helper 2
- Humoral immunity
- Regulators of eosinophils, basophils, and mast cells.

3) Cytotoxic T cell (CD8 – can kill cells directly)
4) T regulator – regulate immune responses

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15
Q

What role do B Lymphocytes (T cells) play in the immune system?

A
  • Play major role in adaptive immunity
  • Lifespan hours – years
  • Mature in bone marrow
    Recognise Ag displayed by antigen presenting cells (APC)
  • Differentiate into plasma cells that make antibodies
    Found in blood, lymph nodes and spleen
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16
Q

What role do natural killer cells play in the immune system?

A
  • Account for 15% of lymphocytes
  • Found in spleen, tissues
  • They recognise and kill cells by apoptosis:
    1) Virus infected cells
    2) Tumours cells
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17
Q

What are soluble factors?

A

Complement, antibodies, cytokines and chemokines

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18
Q

What are complement factors?

A
  • The complement system, is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism
  • It promotes inflammation, and attacks the pathogen’s cell membrane
  • It is part of the innate immune response
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19
Q

What are the three ways complement factors work to enhance the ability of antibodies?

A

1) Lyse microbes directly (membrane attack complex)
2) Increase chemotaxis
3) Opsonisation (C3b – important to remember)

Antibody opsonization is a process by which a pathogen is marked for destruction.

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20
Q

What are antibodies?

A
  • They are the hallmark of adaptive immunity - they bind specifically to antigen
  • Immunoglobulin’s are soluble
  • Ig’s are glycoproteins
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21
Q

What are the 5 distinct classes of immunoglobulins

A

1) IgG

  • Predominant in human serum, 70-75% of total Ig in serum
  • Crosses placenta

2) IgA

  • Accounts for 15% of Ig in serum
  • Predominant Ig in mucous secretions such as saliva, milk and bronchiolar secretions.

3) IgM

  • Accounts for 10% of Ig in serum
  • Mainly found in blood (they’re big so they can’t cross the endothelium)
  • Mainly primary response, initial contact with Ag

4) IgD

  • Accounts for 1% of Ig in serum
  • A transmembrane monomeric form is present on mature B cells

5) IgE
- Accounts for ~0.05% of Ig in serum
- Basophils and mast cells express an IgE-specific receptor that has high affinity for IgE – binding triggers release of histamine
- Associated with allergic response and defence against parasitic infections

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22
Q

What is an antibody?

A
  • A protein produced in response to an antigen.

- It can only bind with the antigen that induced its formation – i.e. specificity.

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23
Q

What is an antigen?

A
  • A molecule that reacts with preformed antibody and specific receptors on T and B cells.
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24
Q

What is an epitope?

A
  • The part of the antigen that binds to the antibody/ receptor binding site
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25
Q

What is affinity?

A
  • The measure of binding strength between an epitope and an antibody binding site.
  • The higher the affinity the better
26
Q

What are cytokines?

A
  • Cytokines are small proteins secreted by immune and non-immune cells
  • They are important in cell signalling
  • Substances produced by one cell that influence the behaviour of another, thus effecting intercellular communication.
27
Q

What are the 4 types of cytokines?

A

1) Interferons (IFN) – induce a state of antiviral resistance in uninfected cells and limit the spread of viral infection

2) Interleukins (IL) –
Can cause cells to divide, to differentiate and to secrete factors

3) Colony stimulating factors (CSF)
Involved in directing the division and differentiation on bone marrow stem cells – precursors of leukocytes

4) Tumour necrosis factors
- Mediate inflammation and cytotoxic reactions

28
Q

What are Chemokines?

A
  • Group of approx. 40 proteins that direct movement of leukocytes from the blood stream into the tissues or lymph organs by binding to specific receptors on cells.
  • They attract leukocytes to sites of infection/inflammation – like magnets
29
Q

What does innate immunity involve?

A
  • Physical and chemical barriers
  • Phagocytic cells (neutrophils and macrophages)
  • Serum proteins (complement, acute phase)
30
Q

What anatomical barriers are present in innate immunity?

A
  • Skin – dermis and epidermis
  • Sebum (skin secretions)
  • Intact skin – prevents penetration, prevents growth
31
Q

What mucous membranes are present in innate immunity?

A
  • Saliva
  • Tears – lysozyme in tears and other secretions
  • Low pH and commensals of vagina
  • Mucous secretions
  • Mucous – entrapment
  • Cilia – beating removes microbes
  • Commensal colonies – attachment, nutrients
32
Q

What physiological barriers are present in innate immunity?

A
  • Temperature – chickens have high body temperature and are Anthrax resistant
  • Fever response inhibits micro-organism growth
  • pH
  • Gastric acidity – neonate stomach less acidic than adult so susceptible to infection
33
Q

Describe the difference between innate and adaptive immunity

A

Adaptive immunity has:

  • Antigen specificity and diversity
  • Immunological memory
  • Specific self/ non-self recognition
  • Whereas innate immunity is non-specific and doesn’t have long-lasting memory
34
Q

Define inflammation

A

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

35
Q

What is the initial response to a barrier being breached?

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
36
Q

What are the hallmarks of the response to inflammation?

A

1) Increased blood supply
2) Increased vascular permeability
3) Increased leukocyte trans-endothelial migration ‘extravasation’
- (extravasation: a discharge or escape, as of blood, from a vessel into the tissues.

Usually lymph from blood into tissues)

37
Q

What is Acute inflammation?

A

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

  • (Resolution – returns to normal homeostatic function)
38
Q

What is Chronic inflammation?

A

Persistent, un-resolved inflammation

39
Q

Describe the process of phagocytosis

A
  • Binding (antibody-antigen)
  • Engulfment
  • Phagosome formation
  • Lysosome fusion (phagolysosome)
  • Membrane disruption
  • Antigen presentation/ secretion
40
Q

What is involved in adaptive immunity?

A
  • Need memory to specific antigen
  • Cell mediated – T cells – intracellular microbes
  • Humoral (Ab) – B cells – extracellular microbes
41
Q

What is a major histocompatibility complex?

A
  • Display peptide from self OR non-self proteins (e.g. degraded microbial proteins) on the cell surface – invasion alert
42
Q

What are the three types of antigen presenting cells?

A
  • Macrophages
  • Dendritic cells (most common)
  • B cells
43
Q

What does cell-mediated immunity require?

A
  • Major histocompatibility complex (MHC)
  • Intrinsic (endogenous) antigens
  • Extrinsic (exogenous) antigens
  • Recognise self or non-self
44
Q

How do T cells (lymphocytes) behave?

A
  • Only respond to intracellular presented antigens

- T cell selection: T cells recognise self are killed in the foetal thymus as they mature

45
Q

How do B cells become activated?

A

1) B cells become activated upon binding with an antigen
2) These then go to the lymph nodes where clonal expansion takes place with the cells differentiating into plasma cells.
3) These secrete antibodies (usually IgM) which later turn into IgG.
4) B cells divide – clonal expansion and differentiate into plasma cells and memory B cells.
- Re-stimulation of memory B cells lead to secondary response.

46
Q

What are the 4 types of hypersensitivity reactions?

A

1) Type 1 - Anaphylactic (IgE)
e. g. Anaphylaxis

2) Type 2- Cell bound (IgG/IgM)
e. g. Pernicious anaemia, Autoimmune haemolytic anaemia, good pastures syndrome, rheumatic fever

3) Type 3 - Immune complex (IgG/IgA)
e. g. SLE

4) Type 4 - Delayed hypersensitivity (T-cell mediated)
e. g. TB, MS

47
Q

Describe anaphylaxis

A
  • It is a Type 1 (IgE) mediated hypersensitivity reaction
  • IgE binds antigen which then cross-links FcεRI on mast cells and basophils leading to massive degranulation and histamine release.
  • Medical emergency that can be fatal.
  • IM Adrenaline is 1st line
  • IV fluids should then be given
  • Chlorphenamine (antihistamine)
  • Hydrocortisone (cortisol) can be used after this.
48
Q

What is the difference between active and passive immunity?

A

ACTIVE IMMUNITY
- Produced by the host immune system

  • Induced by infection or vaccines
  • Durable effective protection
  • Effective after initial lag period
  • Immunological memory is present
  • Boosted effect on subsequent dose

PASSIVE IMMUNITY

  • Passive with no host participation
  • Usually pooled antibodies transferred into the host
  • Transient and less effective
  • No lag period, effective immediately
  • No memory present
  • Subsequent doses do not boost immunity due to elimination
49
Q

What are the problems with immunity?

A
  • Immunity can take a long time but infections arrive quickly and unpredictably
  • Adaptive immunological memory is highly specific, cross-reacting or self-targeting
  • There a lot of bacterial species and viruses out there
  • Only vertebrates have an adaptive system; there must be other effective immune systems
50
Q

What are pattern- recognition receptors?

A
  • Families of receptors exist to detect and recognise microbes and viruses
  • PRRs are present in fluids, cell surfaces, compartments, and intracellularly
  • Respond to pathogens
  • Also have a role in homeostasis and damage recognition
  • Recognise host molecules in autoimmune disease
51
Q

What are Toll-like receptors?

A
  • Involved in the innate immune system
  • Usually expressed on macrophages and dendritic cells
  • They recognize structurally conserved molecules derived from microbes
  • TLR signalling by cellular damage products activates immunity to initiate tissue repair and perhaps enhance local antimicrobial signalling
52
Q

What are the three different types of vaccines used?

A

1) Non-living vaccines
2) Toxoids
3) Live attenuated.

53
Q

Define Passive immunisation

A

Passive immunity is a short-term immunity which results from the introduction of antibodies from another person or animal

54
Q

Define Active immunisation

A
  • Vaccines: antigenic substance prepared from the causative agent of a disease

These can be:

  • Non-living vaccines (whole killed and toxoids)
  • Live attenuated vaccines
55
Q

What are the advantages of passive immunity?

A

Advantages:

  • Gives immediate protection
  • Effective in immunocompromised patients

Disadvantages:

  • Short-lived
  • Possible transfer of pathogens
56
Q

What are non-living vaccines?

A
  • Whole killed vaccines
  • These vaccines do not cause infection but the antigens contained in it induce an immune response which protects against infection.

Limitations:

  • The organisms must be grown to high titre in vitro
  • Whole pathogens often cause excessive reactogenicity
  • Usually need at least 2 vaccinations
57
Q

What is a live attenuated vaccine?

A

The organisms replicate within the host, and induce an immune response which is protective against the wild-type organism

58
Q

What are the advantages and disadvantages of a live attenuated vaccine?

A

Advantages:

  • Lower doses are required, so the scale of in vitro growth needed is lower
  • Immune response more closely mimics that following real infection
  • Route of administration may be more favourable
  • Fewer doses may be required

Limitations:

  • Often impossible to balance attenuation and immunogenicity
  • Reversion to virulence
  • Transmissibility
  • Live vaccines may not be so attenuated in immunocompromised
59
Q

Give some examples of pathogens lacking vaccines.

A
  • HIV
  • Malaria
  • Herpes simplex virus

Because;

  • Pathogen is too hard to grow
  • Killed pathogen not protective
  • Impossible to obtain attenuated and suitably immunogenic strain
60
Q

What are some novel approaches to vaccines?

A
  • Recombinant proteins
  • Synthetic peptides
  • Live attenuated vectors
  • DNA vaccines
61
Q

What are the stages of vaccination?

A

1) Engage the innate immune system
2) Danger signals that activate the immune system, triggers such as molecular fingerprints of infection – PAMPs (pathogen associated molecular patterns)
3) Engage TLR receptors
4) Activate specialist APC
5) Engage the adaptive immune system
a. Generate memory T and B cells
b. Activate T cell help
- During the second exposure, memory T and B cells are generated and circulate for years