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CMB2004 - Cell and Molecular Biology of the Immune System > Lectures 8-11: Immunity and infection > Flashcards

Lectures 8-11: Immunity and infection Flashcards

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1
Q

What are the different organisms that cause disease?

A

Bacteria, viruses, fungi and parasites (worms and protozoa)

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2
Q

What do the different effector mechanisms depend on?

A

Type of pathogen
Localisation
Challenge
Stage of infection

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3
Q

What are the different organisms and protective immunity systems in the interstitial spaces, blood and lymph?

A

Organisms: Viruses, bacteria, protozoa, fungi and worms
Immunity: Antibodies, complement, phagocytosis and neutralisation

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4
Q

What are the different organisms and protective immunity systems in the epithelial surfaces?

A

Organisms: N.gonorrhoeae, M.spp, S.pneumoniae, V.cholerae, E.coli, H.pylori, C.albicans and worms
Immunity: Antibodies (mostly IgA), antimicrobial peptides

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5
Q

What are the different organisms and protective immunity systems in the cytoplasm?

A

Organism: Viruses, C.spp., R.spp., L.monocytogenes and protozoa
Immunity: Cytotoxic T cells and NK cells

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6
Q

What are the different organisms and protective immunity systems in the vesicles?

A

Organism: M.spp., S.typhimurium, Y.pestis, L.spp., L.pneumophila, C.neoforformans, Histoplasma, Leishmania.spp., T.spp.
Immunity: T and NK cell dependent macrophage activation

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7
Q

Why is there no point in antibodies intracellularly?

A

Because most pathogens are extracellular like bacteria

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8
Q

What are the host innate defence mechanisms?

A

Anatomic barriers - skin, oral mucosa, respiratory epithelium and intestine
Complement/antimicrobial proteins - C3, defensives and Regllγ
Innate immune cells - macrophages, granulocytes and NK cells

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9
Q

How do the adaptive and innate immune responses communicate?

A

Using cytokines

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10
Q

What are the different types of CD4+ cells and what are their functions?

A

Th1 - intracellular pathogens, activate macrophages and stimulate cytotoxic T cells
Th2 - extracellular pathogens, support antibody production (class-switching), activate eosinophils, basophils and mast cells
Th17 - extracellular bacteria and fungi, attract inflammatory cells like neutrophils and are induced in early infection

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11
Q

What are the differences between gram positive and negative bacteria?

A

Gram-positive contains a larger area of peptidoglycan whereas gram-negative does not

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12
Q

How do components of bacterial cell walls induce the innate response?

A

Bind to toll like receptors (TLRs) on macrophages
10 TLR genes in humans, recognise distinct molecular patterns on microbes
NOD-like receptors are intracellular sensors that recognise the pathogen

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13
Q

What are NOD-like receptors?

A

Nucleotide binding oligomerisation domains

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14
Q

What are toll-like receptors?

A

Bind pathogen-associated molecular patterns (PAMPs)

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15
Q

What can toll-like receptors do?

A

Promote inflammation
Promote dendritic cell maturation
Influence differentiation of T cells
Activate B cells

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16
Q

What is the ligand and hematopoietic cellular distribution of TLR-1: TLR-2 and TLR-2: TLR-6 heterodimer?

A

Ligands: Lipomannans (mycobacteria), Lipoproteins, lipoteichoic acids, cell-wall β-glucans and zymosan
Cellular distribution: Monocytes, dendritic cells, mast cells, eosinophils and basophils

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17
Q

What is the ligand and hematopoietic cellular distribution of TLR-3?

A

Ligand: double stranded RNA, poly I:C
Cellular distribution: Macrophages, dendritic cells and intestinal epithelium

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18
Q

What is the ligand and hematopoietic cellular distribution of TLR-4?

A

Ligand: LPS and lipoteichoc acids
Cellular distribution: Macrophages, dendritic cells, mast cells and eosinophils

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19
Q

What is the ligand and hematopoietic cellular distribution of TLR-5?

A

Ligand: flagellin
Cellular distribution: Intestinal epithelium, macrophages and dendritic cells

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20
Q

What is the ligand and hematopoietic cellular distribution of TLR-7?

A

Ligand: Single-stranded RNA
Cellular distribution: plasmacytoid dendritic cells, macrophages, eosinophils and B cells

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21
Q

What is the ligand and hematopoietic cellular distribution of TLR-8?

A

Ligand: single-stranded RNA
Cellular distribution: Macrophages and neutrophils

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22
Q

What is the ligand and hematopoietic cellular distribution of TLR-9?

A

Ligand: DNA with unmethylated CpG
Cellular distribution: Plasmacytoid dendritic cells, eosinophils, B cells and basophils

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23
Q

What is the ligand and hematopoietic cellular distribution of TLR-10?

A

Ligand: unknown
Cellular distribution: Plasmacytoid dendritic cells, eosinophils, B cells and basophils

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24
Q

What are bacterias different defence mechanisms against phagocytosis?

A

It may have protective capsules - can be opsonised by antibody/complement (C3B)

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25
Q

How does Streptococcus pneumoniae act?

A

Causes pneumonia, middle ear infection and meningitis
Antibodies to capsular polysaccharides protect against disease
Vaccine has 23 polysaccharide serotypes (out of 91)
Conjugate vaccine

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26
Q

What are the roles of antibodies in bacterial infection?

A

Opsonisation - bind Fc receptors on phagocytes
Complement activation - promote inflammation (C3a, C5a), opsonise by binding C3b receptors on phagocytes, lysis of gram negative organisms
Bind and neutralise toxins
Bind to surface structures preventing mucosal adherence

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27
Q

How is gram negative bacteria killed by complement lysis?

A

Defects in terminal complement components can lead to susceptibility to N.spp.
MAC is not the most important part of complement there defects have more widespread effects (e.g. C3b and C3a+C5a)
Bacterial cell division is vulnerable leading to cell death

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28
Q

What are the different cytokines produced in each type of leprosy?

A

Granulomatous - Th1 cytokines: IL-2 and IFNγ and monokines: TNFα, IL-1β and TGFβ
Lepromatous - Th2 cytokines: IL-4, IL-5 and IL-10

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29
Q

How does the immune system combat bacteria that survive within phagocytes?

A

Th1 response important as cytokines activate macrophages

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30
Q

How are activated macrophages important to the immune system?

A

Better at phagocytosis and killing
More efficient antigen presenting cells
Stimulate inflammation
MHC class I/II and oxygen radicals expressed

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31
Q

What is an example of a response dependent bacterium?

A

Mycobacterium leprae

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32
Q

What are the 2 different types of Mycobacterium leprae?

A

Tuberculoid leprosy: Th1 response, few live bacteria, slow progression and granuloma formation, normal serum immunoglobulin levels
Lepromatous leprosy: Th2 response, large number of bacteria in macrophages, dissemination infection, fatal

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33
Q

What are different visual symptoms of the types of leprosy?

A

Tuberculoid leprosy - skin lesions due to granuloma formation
Lepromatous leprosy - skin involvement with deformities

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34
Q

How do skin lesions form in tuberculoid leprosy?

A

Due to the formation of granuloma containing a core of infected macrophages that becomes necrotic

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35
Q
A
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36
Q

Which different protections are essential for bacterial infection?

A

Antibodies for extracellular pathogens
T cell effector mechanisms for intracellular pathogens

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37
Q

How do virus-infected host cells respond?

A

Type I interferons: IFNα and IFNβ
Resistance to viral replication in all cells by inducting Mx proteins 2’-5’ linked adenosine oligomers and kinase PKR
Increase MHC class I expression and antigen presentation
Activate dendritic cells and macrophages
Activate NK cells to kill virus-infected cells
Induce chemokine to recruit lymphocytes

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38
Q

What does IFN induce the synthesis of?

A

2’,5’ - oligoadenylate synthetase
↓
Adenine trinucleotide synthesised
↓
Activates endonuclease
↓
Degrades viral mRNA

Protein kinase
↓
Phosphorylation and inactivation of eIF-2
↓
Inhibits protein synthesis

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39
Q

How does the synthesis of type I interferons impact viruses?

A

It is induced in virus-infected cells which leads to an early response to infection

40
Q

How does the synthesis of type II interferons impact viruses?

A

IFNγ secreted by activated T cells and NK cells
Inhibits Th2 response and promotes Th1
Recruits macrophages

41
Q

What are the therapeutic uses of interferons?

A

Recombinant IFNα (rIFNα) can be used to treat hepatitis B and C
Used in some cancers
Side effects - very severe (risk of cytokine storm)

42
Q

What are natural killer cells (NK)?

A

Type of innate lymphoid cells
Large granular lymphocytes
Recognise structures on viral infected cells
Can recognise stressed cells in absence of Its and MHC
Kill by extracellular mechanism - perforin and granzyme
Fast

43
Q

How do natural killer cells distinguish between infected and uninfected cells?

A

Activating receptors - recognise carbohydrate ligands triggering killing
Inhibitory receptors - recognises MHC class I molecules

44
Q

What is the cell mediated specific immunity for viruses?

A

Cytotoxic T cells (CD8+) - recognise viral peptide and MHC class I
Cytokines with anti-viral activity - e.g. IFNγ (Class II, activate macrophages)

45
Q

What are the 2 mechanisms of cytotoxic cells killing viruses?

A

Induce apoptosis:
1) secretion of cytotoxic granules
- perforin, polymerises in membrane
- granzymes enter cell
2) Fas ligand on T cell interacts with Fas on target

46
Q

What are CTLs?

A

Cytotoxic T lymphocytes, these act as serial killers when they recognise and bind virus-infected cells which programs death

47
Q

What can CTLs secrete?

A

Cytokines - IFNγ
Inhibit viral replication
Upregulate MHC class I and II expression and antigen presentation
Increase macrophage phagocytosis of dead cells
Promotes NK cell killing activity

48
Q

How do antibodies help target viruses?

A

Neutralise free virus - prevent spread in the body
Opsonise to increase phagocytosis
Activate complement leading to lysis

49
Q

How is influenza targeted by the immune system?

A

Infection induces antibody and cytotoxic T cell (CTL) response
Recognise viral haemagglutinin and neuraminidase
High level CTL activity correlates with reduced viral shedding
Epidemics arise due to new strains

50
Q

How is infection of HIV controlled by higher cytotoxic T cell response?

A

Patients with higher CTL activity show slower disease progression
Virus mutation that escape CTL recognition may lead to progression to AIDS

51
Q

How was knowledge of SARS-CoV-2 used to figure the immune response?

A

Spike glycoprotein (S) binds to ACE 2 receptors on host cell - gain entry
Man to S protein in mince are protected but do not have animal model
High mutation rate
Similar to other coronaviruses
Dampens anti-viral type I infection - viral replication
Inhibit RIG1
Stimulate NFκB activation - pro inflammatory

52
Q

How do parasitic worms (helminths) induce immunity?

A

By inducing a strong IgE antibody response which allows mast cells to mediate inflammation and eosinophil antibody-dependent cell-mediated cytotoxicity

53
Q

How in cell-mediated immunity triggered in parasites?

A

Protozoa survive in macrophages hidden from Igs
Cytokines important in inducing macrophage activation (IL1)

54
Q

How is T cell immunity for Leishmania mediated in mice?

A

BALB/c mice - fatal progressive disease
C57BL/6 mice - resolve infection
Differences in T cell response

55
Q

What are the different evasion mechanisms of pathogens?

A

Concealment of antigens
Antigenic variation
Immunosuppression
Interference with effector mechanisms

56
Q

How can antigens be concealed to evade immune defence?

A

Inhibit antigen presentation by MHC class I ( e.g. herpes simplex and adenovirus)
Privileged sites (latency of Herpes zoster virus in CNS) (hydatid cysts in Echinococcus infection)
Uptake of host molecules ( e.g. schistosomes)

57
Q

How does antigenic variation evade immune defence?

A

Large number of antigenic types (e.g. streptococcus pneumoniae)
Mutation - antigenic drift (e.g. flu, polio, HIV)
Recombination - antigenic shift (e.g. flu)
Gene switching (e.g. trypanosomes)

58
Q

How does Streptococcus pneumoniae evade the immune system?

A

Surrounded by thick polysaccharide capsule which protects it from phagocytosis
Antibodies to the capsule opsonise the bacteria and protect
Leading cause of serious bacterial infection
Causes otitis media, sinusitis, bronchitis and pneumonia

59
Q

What are the main S.pneumoniae vaccines and how do they work?

A

Pneumovax - polysaccharide vaccine not effective in children under 2/ with poor immune function, low level response (B cell)
Prevnar 13 - conjugate vaccine only 13 capsule antigens but bound to diphtheria toxoid highly immunogenic but non-toxic (T and B cell)

60
Q

How does influenza evade the immune response?

A

Antigenic drift (epidemics) and shift (pandemics)
RNA virus, negative sense segmented genome
Infect humans, birds etc.
Epidemics and pandemics
Major surface antigens are haemagglutinin and neuraminidase

61
Q

What is antigenic drift?

A

Neutralising antibodies against haemagglutinin block binding to cells
Mutations alter epitopes in haemagglutinin so that neutralising antibody no longer binds

62
Q

What is antigenic shift?

A

RNA segments are exchanged between viral strains in secondary host
No cross-protective immunity to virus expressing a novel haemagglutinin

63
Q

How does Trypanosoma brucei evade the immune system?

A

Correlates with changes in the major surface antigen of the trypanosome, brought about by genetic rearrangement
Protozoal parasite that causes African sleeping sickness
Spread by Tsetse fly
Patients undergo parasitaemia
Variant-specific glycoprotein (VSG)

64
Q

How does immunosuppression evade immune defence?

A

Infection of immune cells (e.g. HIV-T cells CD4+/ macrophage/dendritic cells)
Induction of regulatory T cells (e.g. chronic infection with H.pylori)

65
Q

What are the factors of regulatory T cells?

A

Type of CD4+ cell
Regulate immune system - suppress differentiation and proliferation of Th1 and Th2
Immunosuppressive (e.g. IL10)
Maintain tolerance of self-antigens
Help prevent autoimmune disease
Express biomarkers CD4 and CD25 on surface and FoxP3 expressed

66
Q

How does Helicobacter pylori evade the immune system?

A

Regulatory T cells may be involved in allowing it to establish a persistent infection
Gram negative bacterium that causes gastric and duodenal ulcers
Found in 1/3 people, causes disease in about 10% of people who are infected

67
Q

How are regulatory T cells induced in Leishmania?

A

Parasite - genus of trypanosomes
Vector - sand fly
Hide and survive in macrophages
Increase expression of T regulatory cells
Decrease immune response

68
Q

How do measles evade the immune response?

A

Causes immunosuppression which can lead to secondary infections
Complications include secondary bacterial respiratory infections
RNA virus; disease is associated with rash commonly accompanied by profound malaise and respiratory symptoms
Shown to infect dendritic cells
Dendritic cells - increased apoptosis, decreased stimulation of T cells, decreased IL-12 production

69
Q

How does the interference with effector mechanisms evade the immune system?

A

Molecules interfere with antibody function (e.g. IgA proteases, Fc-binding molecules)
Molecules interfering with complement (Enzymes that break down C3a/C5a, molecules that inhibit complement activation)
Molecules binding cytokines
Subvert responses by producing molecules with cytokine activity
Inhibition of phagocytic killing

70
Q

What are the innate pathological consequences of immune responses?

A

LPS induces macrophage cytokine secretion (IL1, TNFα via TLR4)
Systemic effects: fever, endotoxic shock, cytokine storms

71
Q

What are the specific pathological consequences of immune response?

A

Antibodies and/or T cell reactions may contribute to pathology (e.g. skin rashes in measles due to T cell response, granuloma formation in TB due to chronic macrophage activation)

72
Q

How does ebola impact the immune response?

A

Filovirus: enveloped, non-segmented negative stranded RNA with filamentous particles
Causes haemorrhage fever
Outbreak West Africa, largest in history
High fatality rate (70% reported)

73
Q

How does ebola evade the immune response?

A

Infects immune cells (dendritic and macrophages)
Inhibits maturation of infected dendritic cells so do not present antigen effectively
Causes apoptosis leading to reduced numbers of circulating T lymphocytes and NK cells and weakened immune responses
Interferes with the production of type I interferon
Interferes with cellular response to interferon

74
Q

What is the immunopathology of ebola?

A

Induction of cytokine storm by macrophages - central role in pathogenesis
Infected macrophages express abundant tissue factor which initiates coagulation cascade - disseminated intravascular coagulation = death

75
Q

What are examples of passive immunity?

A

Hypogammaglobulinaemia in infants as maternal IgG declines
IVIgG very 2-4 weeks for immunodeficiency to maintain protective levels
Tetnus antitoxin

76
Q

What is active immunity?

A

The exploitation of immunological memory
Secondary response is faster to develop and greater in magnitude and may be qualitatively better

77
Q

What is herd immunity?

A

Allows immunisation of the majority of a population which protects the individual and the population (only is most are immunised)

78
Q

What complications can occur in measles?

A

Ear infection - hearing loss
Pneumonia - young children
Sub-acute sclerosing panencephalitis (SSPE) - rare but fatal complication involving the CNS

79
Q

When was the 1st measles vaccine introduced?

A

1963

80
Q

When was the MMR vaccine introduced?

A

1988

81
Q

What percentage of the population needs to be immune to prevent an outbreak?

A

83-94%

82
Q

What are the requirements of an effective vaccine?

A

Safe
High level of protection
Long-lasting protection
Right type of response
Low cost
Stable
Easy to administer
Minimal side effects

83
Q

What are the different types of vaccines?

A

Inactivated - dead
Attenuated - live but virulence disturbed
Subunit - protein fragment
Toxoid - bacterial toxin
Conjugate - low antigenic property covalently bound to something with high

84
Q

What are the features of inactivated vaccines?

A

Important antigens must survive killing
May have side effects
Being replaced by new vaccines

85
Q

What are examples of attenuated vaccines?

A

Vaccina - smallpox
Sabin - polio
MMR - measles mumps and rubella
BCG - tuberculosis

86
Q

What are the pros and cons of live vaccines?

A

Pros:
Single dose effective
May be given my natural route
May induce local and systematic immunity
May induce right type response
Cons:
Reversion to virulence
Possibility of contamination
Susceptible to inactivation
Causes disease in immunocompromised host

87
Q

What are the features of polio?

A

Caused by enterovirus, spread feaco-oral route
Children under 5
1/200 irreversible paralysis
picornaviridae: positive sense RNA
Most infectious subclinical - flu-like symptoms
3 strains
Pakistan and Afganistan

88
Q

What are the features of subunit and toxoid vaccines?

A

Use isolated antigens
Antigen is crucial
May get non-responders
Examples:
Hep B - surface antigen
Pneumococcal polysaccharide - from capsule
Tetnus toxoid - inactivated dorm of protein exotoxin secreted by bacteria

89
Q

What are conjugate vaccines and name examples?

A

Capsular polysaccharide conjugated to protein
Converts TI to TD form
Young children are able to respond
Hib - Haemophilus influenza type B
MenC - meningococcus
Pneumonococcal conjugate

90
Q

What is reverse vaccinology?

A

Whole genome sequencing to identify proteins that could be used as vaccines

91
Q

What vaccine was reverse vaccinology used for?

A

To develop vaccine against Neisseria meningitidis group B

92
Q

What can happen when vaccines cause the wrong type of response?

A

1960s vaccine respiratory syncytial virus (RSV) more serious infection suffered which lead to the death of 2 healthy children

93
Q

What are adjuvants?

A

A substance administered with an antigen to promote immune response
Pure antigens elicit only weak immune response
Enhance the immune responses: provide depot and immunostimulatory properties

94
Q

What are the different ways adjuvants work?

A

Activate dendritic cells via TLRs or NLRs
Release of endogenous danger signals
Promote antigen uptake by dendritic cells
Stimulate release of chemokine/cytokines
Promote cross-presentation of exogenous antigens by class I

95
Q

What is an example of adjuvants in animals and humans?

A

Animals: Freunds adjuvant: oil in water emulsion, complete with mycobacteria
Humans: Alum (aluminium salts), aluminium hydroxide/phosphate licences in 1920s, better for Ab responses than cell mediated immunity

96
Q

Which infections do not have effective vaccines?

A

Malaria
Schistosomiasis
Intestinal worm infestation
Tuberculosis
Diarrheal disease
Respiratory infections
HIV/AIDS

CMB2004 - Cell and Molecular Biology of the Immune System (4 decks)

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