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Introductory Clinical Sciences > Immunology > Flashcards

Immunology Flashcards

1
Q

what are the cells of the innate immune system?

A
  • phagocytes
  • Natural killer cells
  • antigen presenting cells (dendritic cells, macrophages)
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2
Q

what are the cells of the adaptive immune system?

A
  • B lymphocytes

- T lymphocytes

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3
Q

what are the key features of the innate immune system?

A
  • non specific
  • resistance not improved by repeat infection
  • rapid response (hrs)
  • present from birth
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4
Q

what are the key features of adaptive immune system?

A
  • highly specific
  • resistance improved by repeat infection
  • slower response (days-weeks)
  • requires lymphocytes and antibodies
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5
Q

what are some external barriers to infection?

A
  • keratinized skin
  • secretions
  • mucous
  • low pH
  • commensals
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6
Q

what are the soluble factors involved in innate immunity?

A
  • lysosomes
  • complement
  • interferons
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7
Q

what’s the importance of a multipoint haemopoietic stem cell?

A

stem cell that every blood cell in body originate from

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8
Q

give an example of a polymorphonuclear leukocyte

A
  • neutrophils
  • eosinophils
  • basophils
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9
Q

what soluble factors are involved in adaptive immunity?

A

antibodies

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10
Q

what is the purpose of pattern recognition receptors?

A

to discriminate self from non-self by recognising unchanging patterns of microbes

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11
Q

how do pattern recognition receptors work? (on a basic level)

A

recognise conserved polysaccharide molecular patterns on microbes - patterns that are constant across a group of bacteria

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12
Q

what do pattern recognition receptors activate?

A

innate immune system –> damage recognition receptors on dendritic cells

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13
Q

what are cell associated PPRs?

A
  • receptors present on the cell membrane of in the cytosol of the cell
  • able to recognise a broad range of molecular patterns
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14
Q

give an example of a PPR

A

TLR (toll like receptor) are main family –> recognise different bugs and respond to damage in cells

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15
Q

EXTRA .. what does TLR4 bind to?

A
  • lipopolysaccharide in bacterial walls
  • pneumolysin
  • viral proteins
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16
Q

when activated, what do TLRs do?

A
  • induce signal transduction and cellular events, leading to induction of pro-inflammatory cytokines
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17
Q

what are the 2 (broad) type of PRRs?

A
  • secreted and circulating PRRs

- cell associated PRRs

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18
Q

describe the structure of an antibody?

A
  • two Fab regions attached to an Fc region by a hinge

Fab = variable sequence
Fc = constant
2 light chains and 2 heavy chains

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19
Q

what’s does Fab bind to?

A

specific antigens

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20
Q

what does Fc region bind to?

A

complement, Fc receptors on phagocytes, NK cells etc

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21
Q

what are the 5 classes of Ig’s?

A 
IgG
IgA
IgM
IgE
IgE
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22
Q

what is the function of IgG antibodies?

A
  • most predominant in human serum .. 70-75% total serum Ig
  • able to cross placenta
  • binds to complement
  • important in secondary/ memory responses.
  • main effector of humoral immunity
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23
Q

what is the function of IgM?

A
  • low affinity and specificty
  • important in primary
  • response - first line defence
  • mainly found in blood and too big to cross endothelium
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24
Q

what is the function of IgA?

A
  • predominant Ig in mucous secretions

- protects mucosal surfaces

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25
Q

what is the function of IgE?

A
  • Basophils and mast cells express IgE specific receptor with high affinity for IgE and binding triggers histamine release
  • present at low levels
  • involved in allergy response + parasitic infections
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26
Q

outline the process of phagocytosis

A
  1. Binding
  2. Engulfment
  3. Phagosome formation
  4. Lysosome fusion (phagolysosome)
  5. Membrane disruption
  6. Antigen presentation/ secretion
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27
Q

how does specific antibody Fab binding protect against infection?

A
  • neutralize toxins
  • immobilise motile microbes
    prevent binding to host cells
  • form complexes - (each Ig can bind 2 pathogens)
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28
Q

how do antibodies enhance innate mechanisms to protect against infection (Fc)?

A
  • Activate complement
  • bind Fc receptors on:
    phagocytes - enhanced phagocytosis
    mast cells - inflammatory mediator release.
    NK cells - enhance killing of infected cells
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29
Q

what are the 4 main types of T-cell?

A

T helper 1 (CD4 – help immune response to intracellular pathogens)

T helper 2 (CD4 – help produce antibodies to extracellular pathogens)

Cytotoxic T cell (CD8 – can kill cells directly)

T-regulator (regulate immune response)

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30
Q

what is the role of a t-helper cell?

A
  • help B cells make antibody
  • activate macrophages and NK cells
  • help development of cytotoxic T cells
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31
Q

describe the structure of a t-cell receptor

A

a heterodimer of either alpha/beta or gamma/delta chains.
similar to Fab arm of antibody.
each one is specific to an antigen

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32
Q

how do t-cell receptors recognise antigens?

A

recognise antigen peptides in context of MHC class I and II antigens

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33
Q

which MHC classes do T helper cells recognise?

A

MHC class II - use CD4

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34
Q

which MHC classes do cytotoxic T cells recognise?

A

MHC class I - use CD8

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35
Q

which cells are MHC I and MHC II expressed by?

A

MHC I = all nucleated cells

MHC II = antigen presenting cells (macrophages, dendritic cells + B cells)

36
Q

which T cells do MHC I and MHC II display antigens to, respectively?

A

MHC I displays them to CD8+ (cytotoxic) T cells.

MHC II = CD4+ (helper) T cells

37
Q

briefly describe the process of antigen presentation to cytotoxic T cells

A
  1. virus infects cell
  2. viral proteins are broken down in cytosol.
  3. peptides transported to ER, bind MHC I
  4. transported to cell surface
  5. activated cytotoxic T cells kill infected cell by inducing apoptosis
38
Q

briefly describe the process of antigen presentation to T helper cells

A
  1. macrophage/dendritic cell/B cell internalises and breaks down foreign material
  2. peptides bind to MHC II in endosomes
  3. transported to cell surface
  4. activated T helper cells help B cells make antibody, and produce cytokines that activate/regulate other leukocytes
39
Q

what are cytokines?

A

proteins secreted by immune and non immune cells –> substances produced by one cell that influence the behaviour of another, affecting intercellular communication

40
Q

how do cytokines act?

A

by binding to specific receptors on surface of target cells

41
Q

list some groups of cytokines?

A
  • interferons
  • interleukins
  • colony stimulating factors
  • tumour necrosis factors
42
Q

what do TH1 cells do?

A
  • activate macrophages, cause inflammation
  • promote production of cytotoxic T cells (cell-mediated immunity)
  • important in intracellular infections
  • induce B cells to make IgG antibodies
43
Q

what do TH2 cells do?

A
  • activate eosinophils and mast cells
  • important in allergy
  • induce B cells to make IgE - promotes release of inflammatory mediators e.g. histamine from mast cells
44
Q

what is an epitope of an antigen?

A

portion of the antigen that is bound by antibody

45
Q

what bonds might form between and antigen and antibody?

A
  • charge interactions
  • hydrophobicity
  • van der waals
  • hydrogen bonds
46
Q

what is opsonisation?

A

coating of pathogens by antibody, leading to increased phagocytosis

47
Q

where do B cells mature?

A
  • mature in bone marrow

- found in blood, lymph nodes and spleen

48
Q

what do macrophages do?

A
  • reside on tissue and are often first line of non-self recognition e.g. Kupffer cells
  • present antigen to T cells
49
Q

where are natural killer cells found?

A

spleen and tissues

- recognise and kill birds infected cells/tumour cells by apoptosis

50
Q

briefly outline the stages of phagocytosis

A
  1. Binding
  2. Engulfment
  3. Phagosome formation
  4. Lysosome fusion (phagolysosome)
  5. Membrane disruption
  6. Antigen presentation/ secretion
51
Q

what is passive immunisation?

A

transfer of preformed antibodies to the circulation.

  • can be natural or artificial
  • e.g. breastmilk, immunoserum again pathogens
52
Q

what is active immunisation?

A
  • causes immune system to induce production of high affinity antibodies
  • safely mimics natural infection
  • induction of immunological memory
53
Q

give some advantages and disadvantages of passive immunisation?

A

Advantages:
• Gives immediate protection
• Effective in immunocompromised patients

Disadvantages:
• Short-lived
• Possible transfer of pathogens

54
Q

what are the types of vaccine used?

A

non living –> whole killed and toxoids (inactivated toxins)

live attenuated

55
Q

why might a pathogen not have an available vaccine?

A
  • pathogen is too hard to grow
  • killed pathogen isn’t protective
  • impossible to obtain attenuated and suitably immunogenic strain
56
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 antigen presenting cells
  5. Engage the adaptive immune system  Generate memory T and B cells + Activate T cell help
57
Q

what are the indications for using artificial passive immunity?

A
  • individuals with B cell defects
  • exposure to disease at risk of complication
  • no time for active immunisations
  • pathogen with short incubation period
  • acute danger of infections
58
Q

what do anti-toxins do?

A
  • give passive immunity as with some pathogens, toxins released are the main hazard (not primary infection)
    e. g. tetanus
59
Q

what is inoculation?

A

vaccination involving introduction of a viable microorganism into the subject

60
Q

what would be a ‘perfect’ vaccine?

A
  • achieving long term protection from a small number of immunisations
  • stimulate B and T cells
  • induce memory b and T cells
  • stimulate protective high affinity IgG production
61
Q

describe the primary immune response

A
  • relies on innate immunity
  • IgM predominates
  • low affinity
62
Q

describe the secondary immune response

A
  • rapid, large reaction
  • high affinity IgG
  • T cells help
  • doesn’t rely on innate immune system
63
Q

discuss advantages + disadvantages of live attenuated vaccines

A

advantages

  • full immune response activate
  • prolonged contact with immune system
  • stimulations of B and T cell memory
  • often 1 injection

disadvantages

  • can cause infection in immunocompromised patients
  • complications
  • could cause outbreak in poor sanitation
  • requires refrigeration and transport
64
Q

discuss advantages + disadvantages of whole inactivated pathogen vaccines?

A

advantages

  • no infection risk
  • less complicated storage that L.A
  • can get good immune response

disadvantages

  • just activate humeral response with lack of T-cell response
  • booster vaccinations needed as response is often weak
  • can lead to issue with compliance
65
Q

discuss advantages + disadvantages of subunits vaccines (e.g. toxoids, recombinant proteins, purified proteins + capsular polysaccharides)

A

advantages

  • safer than live/inactivated pathogens
  • no infection risk
  • easy to store + preserve

disadvantages

  • less powerful immune response
  • repeat vaccinations needed
66
Q

how does a DNA vaccine work?

A
  • transiently expresss genes from pathogens in host cells + generate immune response (T and B memory)
    BUT no transient infection causes so produce mild response and requires boosters
67
Q

how does a recombinant vector vaccine work?

A
  • imitate effect of transient pathogen infection using a non pathogenic organisms
  • genes for pathogen antigens introduced into non pathogenic microorganism and introduced to host
68
Q

name immunoglobulin typically involved in allergy?

A

IgE (can involved IgG and IgA)

69
Q

define allergy

A

abnormal response to harmless foreign material

70
Q

what cells are involved in allergy?

A

mast cells
eosinophils
lymphocytes
dendritic cells

effectors –> smooth muscle, fibroblasts + epithelia

71
Q

what cells express high affinity IgE receptors?

A
  • eosinophils
  • mast cells
  • basophils
72
Q

what cell express low affinity IgE receptors?

A
  • B cells
  • T cells
  • monocytes
  • eosinophils
  • platelets
  • neutrophils
73
Q

list some indirect activators of mast cells?

A

act via IgE

  • allergens e.g. wasp venom
  • bacterial/viral antigens
  • phagocytosis of enterobacteria
74
Q

list some direct activators of mast cells?

A
  • cold
  • aspirin
  • latex
75
Q

briefly outline some key characteristics of anaphylaxis?

A
  • occurs in minutes to hours
  • involves mast cell or basophils activation (IgE or direct )
  • histamine and trptase are elevated
  • causes vasodilation, increased vascular permeability, low BP, bronchoconstriction, rash, swelling, GI pain, vomiting etc.
76
Q

what is type I hypersensitivity reaction?

A
  • immediate hypersensitivity
  • due to activation of IgE antibody on mast cells or basophils
  • acute anaphylaxis
77
Q

what is type II hypersensitivity reaction?

A
  • antibody to cell bound antigen
  • triggered by antibodies reacting with antigenic determinants on cell membrane of target tissue
  • body treats it as foreign protein and forms antibody
78
Q

what is a type III hypersensitivity reaction?

A
  • immune complex hypersensitivity
  • results from deposition/ formation of immune complexes in tissues
  • small blood vessels damaged or blocked
79
Q

what is a type IV hypersensitivity reaction?

A
  • delayed hypersensitivity
  • mediated by t-lymphocytes reacting with antigen –> sensitisation
  • second challenge results In delayed reaction (local inflammation taking 2-3 days to develop)
80
Q

what is the complement system?

A
  • a series of interacting plasma proteins acting in a cascade
  • major effector system for antibody mediated immune response
81
Q

what are the 3 pathways complement can be activated by?

A

1 - classical pathway –> by antibody
2 - alternative pathway –> by bacterial cell walls
3 - lectin pathway –> by mannose binding lectin

82
Q

what are the effectors of complement activation?

A
  • increased vascular permeability
  • chemoattraction of leukocytes
  • enhanced phagocytosis
  • cell lysis
83
Q

how is complement activation controlled?

A
  • spontaneous decay of exposed attachment sites

- inactivation by specific inhibitors

84
Q

what is the major purpose of complement pathway?

A
  • remove or destroy antigen by direct lysis or opsonisation
85
Q

what are the 2 stages of complement activation?

A

1 activation of C3

2 activation of lytic pathway

Introductory Clinical Sciences (5 decks)

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