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MBB163 > Partridge (Immune System) > Flashcards

Partridge (Immune System) Flashcards

1
Q

What is immunology?

A
  • study of immune system
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2
Q

What is immune system?

A
  • integrated system of cells and molecules that defend against disease, by reacting against infections
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3
Q

What is the medical importance of immunology?

A
  • vaccination
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4
Q

Examples of malfunctions in immune system?

A
  • immunodeficiency
  • allergy
  • autoimmune disease
  • graft rejection
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5
Q

What are immunological techniques?

A
  • research, diagnostics, therapeutics
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6
Q

How do bacteria carry out immune surveillance?

A
  • restriction enzymes
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7
Q

How do invertebrates carry out immune surveillance?

A
  • negative surveillance, cells marked w/ “self” protein labs, unlabelled non-self cells destroyed by phagocytes
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8
Q

How do vertebrates carry out immune surveillance?

A
  • external barriers (skin)
  • negative surveillance by major histocompatibility complexes, v polymorphic
  • positive surveillance specific recognition of foreign cells (active immunity)
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9
Q

What is the difference between innate and adaptive immune system?

A
  • innate has broad specificity and adaptive highly specific
  • in innate resistance resistance not improved by repeat infection, but is in adaptive
  • innate has rapid response (hrs) and adaptive has slower response (days-wks)
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10
Q

What does 2º contact w/ antigen result in?

A
  • enhanced adaptive responses
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11
Q

What are the external barriers to infection?

A
  • keratinised skin –> keratin difficult for bacteria to digest and must be damaged to infect
  • secretions –> sebum, sweat, FAs, lactic acid, lysosyme = low pH, dry and salty
  • mucous –> cilia in resp tract traps pathogens
  • low pH of 2.5 in stomach
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12
Q

What is commensalism?

A
  • 1 organism benefits from another
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13
Q

What are the 3 types of phagocytes?

A
  • neutrophils
  • mononuclear phagocytes
  • mast cells
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14
Q

What are the characteristics and role of neutrophils?

A
  • main phagocyte in blood
  • short-lived
  • fast moving
  • lysosomes release enzymes (H2O2) etc.
  • unusual shaped nucleus
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15
Q

What are the characteristics and role of mononuclear phagocytes?

A
  • monocyte in blood/macrophage in tissue
  • long lived (months-yrs)
  • help initiate adaptive responses
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16
Q

What are the characteristics and role of mast cells?

A
  • underlying mucosal surfaces in skin
  • release inflammatory mediators (eg. histamine)
  • important in parasite and allergy response
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17
Q

What are the characteristics of NK cells?

A
  • type of lymphocyte
  • kill virally infected cells non-specifically
  • important in self/non self recognition and may kill cancer cells
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18
Q

How are pathogens recognised by phagocytes/mast cells? (innate)

A
  • have general pathogen recognition receptors (PRRs)
  • that recognise pathogen-assoc molecular pattern (PAMPs)
  • eg. Toll-like receptor 4 recognises LPS
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19
Q

How are pathogens recognised by NK cells? (innate)

A
  • kills target unless they recognise self protein (MHCI)
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20
Q

What are the integrated responses to infection/injury?

A
  • inflammation (v beneficial), localised response to infection and damage (dilation of blood vessels, increase in capillary permeability, phagocytes migrate into tissue)
  • PAMPS/DAMPS (pathogen/damage assoc mol pattern)
  • induces release of inflammatory mediator and prod of cytokines
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21
Q

3 examples of soluble factors

A
  • complement system
  • defensins
  • interferons
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22
Q

What is the complement system?

A
  • approx 20 proteins in blood
  • activated on infection
  • bacterial cell lysis
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23
Q

What are defensins?

A
  • positively charged peptides
  • made by neutrophils
  • disrupt bacterial membranes
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24
Q

What are interferons?

A
  • prod by virally infected cells
  • protect uninfected cells
  • activate macrophages and NK cells
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25
Q

What are soluble factors also involved in?

A
  • cell to cell communication
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26
Q

What are cytokines?

A
  • ‘hormones of immune response’
  • eg. interleukins (act between WBCs)
  • prod by cells of innate and adaptive IS
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27
Q

Example of inflammatory mediator?

A
  • histamine
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28
Q

How is temp response (fever) an example of an acute phase response?

A
  • on infection, macrophages may release interleukin 1 (IL-1)
  • acts on hypothalamus
  • increases temp
  • stimulates phagocytosis
  • decreases Fe levels in blood
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29
Q

How are antigens recognised by adaptive IS?

A
  • by specific receptors on T and B lymphocytes
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30
Q

Where do B and T lymphocytes mature and then move to?

A
  • B mature in bone marrow
  • T mature in thymus
  • move to central lymphoid tissue (antigen independent differentiation)
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31
Q

What occurs during maturation of lymphocytes?

A
  • acquire antigen receptors
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32
Q

What is the difference between the receptors of B and T lymphocytes?

A
  • B are antibodies

- T are T cell receptors

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33
Q

What type of differentiation occurs in peripheral lymphoid tissue?

A
  • antigen dependent differentiation
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34
Q

What is the role of B lymphocytes, type of immunity they provide and infections they work against?

A
  • secrete antibodies
  • humoral immunity
  • for extracellular bacterial and 2º viral infection
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35
Q

What is the role of T lymphocytes, type of immunity they provide and infections they work against?

A
  • kill infected host cells
  • make cytokines
  • cell mediated immunity
  • for viral, intracellular bacterial and intracellular parasitic
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36
Q

What was the role of Jenner in immunology?

A
  • developed vaccination principles
  • showed infection w/ cowpox protected against smallpox
  • as shared antigens
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37
Q

What does the cell mediated (T cell) immune response involve?

A
  • clonal expansion, differentiation, memory

- T cells can only recognise antigen bound to host cell

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38
Q

What is the clonal selection hypothesis?

A
  • millions of B cells prod
  • when 1 w/ correct antibody binds to antigen, triggers clonal selection of this cell
  • lymphocytes that recognise “self” deleted early in dev
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39
Q

What are the types of vaccine?

A
  • subunit, eg. toxoid (from toxin)

- attenuated strains

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40
Q

How is lymphoid tissue organised?

A
  • 1ºis where lymphocytes reach maturity

- 2º is where mature lymphocytes stimulated by antigen, clustered around places of entry

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41
Q

What is humoral (antibody) immunity?

A
  • antigen –> B lymphocytes (antibody receptor) –> plasma cells –> soluble antibody
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42
Q

What class do antibodies belong to?

A
  • class of soluble glycoproteins, called immunoglobulins
43
Q

How does an antibody’s structure reflect its dual role in immune response?

A
  • antigen recognition = Fab regions variable in seq and binds diff antigens specifically
  • antigen elimination = Fc region constant seq, binds to component, Fc receptors on phagocytes and NK cells etc.
44
Q

What is the role of antibodies?

A
  • act as labels for infectious material

- labelled material “eliminated”

45
Q

What do Fab and Fc mean?

A
  • Fab = fragment antigen binding

- Fc = fragment crystallisable

46
Q

How do the sizes vary between the light chain, heavy chain and total molecule?

A
  • L = 25kD
  • H = 50kD
  • L2H2 (immunoglobulin G) = 150kD
47
Q

What AA is the hinge range rich in, and why?

A
  • Pro
  • so flexible
  • but susceptible to proteolytic digestion
48
Q

What are the 5 immunoglobulin classes of H chain and how do they differ?

A
  • IgG (γ)
  • IgM (μ)
  • IgA (α)
  • IgD (δ)
  • IgE (ε)
  • differ in AA seq of H chains
49
Q

What are the 2 types of L chain and are they class restricted?

A
  • kappa (κ)
  • lambda (λ)
  • no, can have IgGκ or IgGλ antibodies
50
Q

What is the variable region of an antibody?

A
  • binds antigen

- differ between antibodies w/ diff specificities

51
Q

What is the constant region of an antibody?

A
  • same for all antibodies of given H chain class of L chain type
52
Q

Are the variable and constant regions of an antibody encoded by the same exon?

A
  • no, encoded by separate exons
53
Q

How can multiple variable regions in genome give diff antibody specificities?

A
  • regions can recombine and mutate during B cell differentiation
54
Q

How do H chain classes differ in 2º response?

A
  • can include IgA and IgE
  • same amount of IgM
  • much more IgG
55
Q

How do antibodies use specific binding/valency to protect against infection, and what H chain classes do these involve?

A
  • Fab region
  • neutralise, eg. toxins (IgG, IgA)
  • immobilise mobile MOs (IgM)
  • prevent binding to and infection of host cells
  • form complexes, cross link antigens on diff pathogens to clump them together, so easier to deal w/
56
Q

How do antibodies use effector functions to protect against infection, and what H chain classes do these involve?

A
  • Fc region
  • activate complement (IgG, IgM)
  • bind Fc receptors, phagocytes (IgG), mast cells (IgE), NK cells (IgG)
57
Q

What does the complement induce?

A
  • inducer of inflammation, can cause pathology
58
Q

How are serum proteins activated in complement?

A
  • 20 serum proteins activated via enzyme cascade
59
Q

How is the complement activated?

A
  • specifically by antigen/antibody complexes (classical pathway)
  • or non-specifically, by eg. certain bacteria (MB-lectin or alternative pathway)
60
Q

What are the 3 major biological activities of the complement?

A
  • activation
  • opsonisation
  • cell lysis
61
Q

What happens during activation by complement?

A
  • phagocyte recruitment
  • induces inflammation
  • C5a (or C3a)
  • chemoattractants (causes chemotaxis)
  • anaphylatoxins (mast cells release lots of inflammatory mediators all over body)
62
Q

What happens during opsonisation by complement?

A
  • C3b binding and phagocytosis
  • C3b binds to bacterium membrane
  • phagocytes have receptors, so can be bound w/ high affinity and destroyed more efficiently
63
Q

What happens during cell lysis by complement?

A
  • need activation of whole cascade

- membrane attack complex: C9 –> polymers –> hollow cylinders which form pores in bacterial membranes

64
Q

What is involved in the classical pathway? (complement)

A
  • req Ag/Ab2, C1, C2, C4
  • 2 IgG molecules attached to bacterial cell surface
  • C1 must interact w/ 2 Fc regions
  • IgM more potent activator of complement (pentamer)
65
Q

What is the role of Fc receptors on phagocytes?

A
  • IgG and IgA most important
  • some classes of antibodies can act as opsonins
  • pseudopods fuse to form phagosome and release contents
  • phagolysosome acid, peptides, toxic O derivatives, competitor enzymes
66
Q

What is the role of Fc receptors on NK cells?

A
  • only IgG has receptors on NK cells
  • mediate antibody dependent cell-mediated cytotoxicity (ADCC)
  • secrete perforin from granules, allows passage of particles to induce apoptosis
  • target undergoes apoptosis, cell contents destroyed and “corpse” taken up by macrophages
67
Q

What is the role of Fc receptors on mast cells?

A
  • IgE
  • mediate allergy and defence against large particles
  • allergen binds to specific IgE, causing degranulation, which releases inflammatory mediators, eg. histamine, causing local inflammation
  • beneficial in response to particles
68
Q

What is an epitope?

A
  • antibodies of similar structure
69
Q

How is antisera production used in research and medicine?

A
  • conventional antisera = polyclonal antisera
  • used to give 2º response (IgG in animals)
  • remove small amount of blood and allow to clot
  • may lack fine specificity and difficult to standardise
70
Q

How are monoclonal antibodies used in research and medicine?

A
  • single specificity (binds 1 epitope)
  • derived from single B lymphocyte
  • B cells from animal immunised w/ antigen A and isolated
  • B cells fused w/ tumour cell line (divide indefinitely)
  • prod hybrid cells, make anti-A antibody
71
Q

How are antibodies used in research, diagnostics and therapy?

A
  • identifying and labelling molecules in complex mixtures
  • serotyping pathogens
  • characterising cell surface proteins, identifying cell types
  • “humanised” antibodies, used in therapy, magic bullets to kill cancer cells
72
Q

What are the 2 major sub pops of T cells and what are their roles?

A
  • T helper cells –> help B cells make antibodies, activate macrophages and Nk cells, help dev of cytotoxic T cells
  • T cytotoxic cells –> recognise and kill infected host cells
73
Q

What is the structure of T lymphocyte receptor (TCR) and how does this relate to its function?

A
  • v similar to Fab arm of antibody

- variable regions responsible for antigen recognition

74
Q

What do B and T cells recognise?

A
  • B recognise “soluble” free native antigens
  • T recognise “cell-assoc” processed antigens
  • cytotoxic T cells recognise peptide bound to MHCI
75
Q

What happens during T cell recognition of antigen?

A
  • viral proteins in a virus infected cell broken down in cytosol (proteasomes)
  • peptides transported to ER, bind MHCI w/ cell surface
  • activated cytotoxic T cells kill infected cell by inducing apoptosis
  • helper T cells recognise protein bound to MHCII
  • macrophage/dendritic cell/B cell internalises and breaks down foreign material
  • peptides bind to MHCII in endosomes on cell surface
  • activated T helper cells help B cells make antibody and prod cytokines that activate/reg other leucocytes
76
Q

What is the problem w/ lymphocytes meeting antigen?

A
  • lymphocyte w/ specific receptor must meet antigen
77
Q

What is lymph?

A
  • extracellular fluid that accum in tissues and carried by lymphatic vessels back through lymphatic system to thoracic duct and into blood
78
Q

Where is adaptive immunity activated?

A
  • in draining lymph node
79
Q

What encodes major histocompatibility proteins?

A
  • major histocompatibility gene complex (MHC)

- chromosome 6

80
Q

What is the role of major histocompatibility proteins?

A
  • initiating T cell responses

- important in graft rejection

81
Q

Are major histocompatibility proteins polymorphic, and what does this mean?

A
  • yes, v polymorphic
  • most polymorphic proteins in man
  • many diff alleles at each gene locus
82
Q

Where are major histocompatibility proteins expressed?

A
  • MHCI on all nucleated cells, displays antigen to CD8+ve (cytotoxic T cells)
  • MHCII on macrophages, dendritic cells and B cells, displays antigen to CD4+ve (helper T cells)
83
Q

What are cytokines and what is their role?

A
  • small (approx 5-20kD) secreted proteins
  • involved in communication between cells of immune response
  • can have autocrine or paracrine activity
  • usually prod and act locally
  • act by binding to specific receptors on target cell surface
84
Q

What are the main groups on cytokines and their roles?

A
  • interleukins (IL-1 - IL-38?) –> usually made by T cells
  • interferons (IFNs) –> viral infections, cell activation
  • chemokines –> cell movement or chemotaxis
  • colony stimulating factors (CSFs) –> leucocyte prod
85
Q

What cytokines do diff types of T helper cells prod?

A
  • TH1 cells –> inflammatory intracellular infections, prod IL-2, γ-interferon and TNFβ
  • TH2 cells (parasitic) –> prod range of interleukins
  • TREGs, suppress other T cells
86
Q

How does HIV infect cell?

A
  • 2 copies ss RNA enter cyto
  • RNA to DNA by reverse transcriptase
  • takes part of host cell as it leaves, creating envelope, gp120 = viral receptor
  • virus binds to cell receptor
  • virus envelope fuses w/ plasma membrane
  • nucleocapsid enters cyto
  • viral RNA reverse transcribed into ds DNA
  • viral DNA transported to nucleus and integrated into host cell genome (provirus)
  • new viral genomic RNA and mRNA transported to cyto
  • viral mRNA translated to viral protein
  • new nucleocapsids form and virus “buds” from cell
  • acquires lipid envelope
87
Q

Which cells and how many are infected by HIV?

A
  • CD4+ve cells susceptible to infection
  • no. T cells infected increases w/ each round of viral rep
  • monocytes, macrophages and dendritic cells also infected, as low levels CD4+ve
88
Q

How does latent HIV infection progress?

A
  • T cell stimulation activates HIV provirus transcrip

- T cell lysis

89
Q

How do dendritic cells and monocytes respond to HIV infection?

A
  • dendritic cells present antigen to T cells in lymphoid tissue
  • monocytes may traverse blood/brain barrier, CNS involvement
90
Q

How can CD4 expression affect HIV infection?

A
  • not sufficient for HIV infection
  • but may influence susceptibility to infection/disease progression
  • progression slower if young and healthy
  • some not susceptible as no chemokines
91
Q

What are the co-receptors for the HIV virus?

A
  • chemokine receptors
92
Q

How do symptoms of HIV progress to AIDS?

A
  • ‘flu-like’ symptoms
  • (seroconversion occurs)
  • asymptomatic
  • symptomatic
  • AIDS
  • death
93
Q

What is the immune response to HIV?

A
  • high levels of virus in blood initially cleared (mainly by cytotoxic T cells)
  • antibodies may not be detected for 3-6 months (seroconversion) –> B may not be helped by T helper cells
  • IS mounts vigorous response against virus, CD8+ve cytotoxic T cells esp important
94
Q

How does HIV avoid immune detection?

A
  • mutates
95
Q

What does T helper cell depletion lead to immune response against HIV?

A
  • direct lysis by virus
  • killed by cytotoxic T cells or other immune mechanisms
  • infected cells in lymphoid tissue
96
Q

What are the symptoms of AIDS?

A
  • opportunistic infections, eg. Candida
  • reactivation of latent infections
  • rare cancers (caused by viruses)
  • CNS involvement, dementia
  • all adaptive immune response compromised
97
Q

What do the symptoms of AIDS show about T helper cells and how?

A
  • that they’re vital in IS

- as memory T cells lost

98
Q

What are the differences between HIV-1 and HIV-2?

A
  • HIV-2 slower to progress to AIDS

- HIV- 2 predates HIV-1

99
Q

How is HIV transmitted?

A
  • unprotected sex (approx 70%)
  • blood/blood products (mainly IV drug use, approx 28%)
  • breast feeding
  • mother to foetus
100
Q

How can HIV/AIDS be prevented through changes in behaviour?

A
  • blood testing
  • safe sex
  • decrease in IV drug use/needle sharing
  • treating HIV +ve pregnant women
101
Q

What are the problems with preventing HIV/AIDS through vaccination?

A
  • difficult due to high mutation rate
  • humoral immunity may not be productive
  • need to induce cytotoxic T cells (some people never progress to AIDS due to elite ones)
102
Q

How can HIV/AIDS be prevented through drug therapy and what are the problems?

A
  • problems = high mutation rate, toxicity, viral latency, cost
  • combo therapy = 3+ drugs directed at diff viral targets
  • no. infected hasn’t decreased much
103
Q

What future treatments could be available for AIDS?

A
  • gene editing
  • immunisation of infected patients, “kick and kill”
  • possible immunisation using human monoclonal antibodies

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