Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

Lectures 8-11: Immunity and infection Flashcards

(99 cards)

Start Studying
1
Q

What are the different organisms that cause disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do the different effector mechanisms depend on?

A

Type of pathogen
Localisation
Challenge
Stage of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is there no point in antibodies intracellularly?

A

Because most pathogens are extracellular like bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do the adaptive and innate immune responses communicate?

A

Using cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are NOD-like receptors?

A

Nucleotide binding oligomerisation domains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are toll-like receptors?

A

Bind pathogen-associated molecular patterns (PAMPs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can toll-like receptors do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is bacterias defence mechanism against phagocytosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
How does Streptococcus pneumoniae act?
Causes pneumonia, middle ear infection and meningitis Antibodies to capsular polysaccharides protect against disease Vaccine has 23 polysaccharide serotypes (out of 91) Conjugate vaccine
26
What are the roles of antibodies in bacterial infection?
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
27
How is gram negative bacteria killed by complement lysis?
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
28
What are the different cytokines produced in each type of leprosy?
Granulomatous - Th1 cytokines: IL-2 and IFNγ and monokines: TNFα, IL-1β and TGFβ Lepromatous - Th2 cytokines: IL-4, IL-5 and IL-10
29
How does the immune system combat bacteria that survive within phagocytes?
Th1 response important as cytokines activate macrophages
30
How are activated macrophages important to the immune system?
Better at phagocytosis and killing More efficient antigen presenting cells Stimulate inflammation MHC class I/II and oxygen radicals expressed
31
What is an example of a response dependent bacterium?
Mycobacterium leprae
32
What are the 2 different types of Mycobacterium leprae?
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
33
What are different visual symptoms of the types of leprosy?
Tuberculoid leprosy - skin lesions due to granuloma formation Lepromatous leprosy - skin involvement with deformities
34
How do skin lesions form in tuberculoid leprosy?
Due to the formation of granuloma containing a core of infected macrophages that becomes necrotic
35
Which different protections are essential for bacterial infection(intracellular and extracellularly)?
Antibodies for extracellular pathogens T cell effector mechanisms for intracellular pathogens
36
How do virus-infected host cells respond?
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
37
What does IFN induce the synthesis of?
2',5' - oligoadenylate synthetase ↓ Adenine trinucleotide synthesised ↓ Activates endonuclease ↓ Degrades viral mRNA Protein kinase ↓ Phosphorylation and inactivation of eIF-2 ↓ Inhibits protein synthesis
38
How does the synthesis of type I interferons impact viruses?
It is induced in virus-infected cells which leads to an early response to infection
39
How does the synthesis of type II interferons impact viruses?
IFNγ secreted by activated T cells and NK cells Inhibits Th2 response and promotes Th1 Recruits macrophages
40
What are the therapeutic uses of interferons?
Recombinant IFNα (rIFNα) can be used to treat hepatitis B and C Used in some cancers Side effects - very severe (risk of cytokine storm)
41
What are natural killer cells (NK)?
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
42
How do natural killer cells distinguish between infected and uninfected cells?
Activating receptors - recognise carbohydrate ligands triggering killing Inhibitory receptors - recognises MHC class I molecules
43
What is the cell mediated specific immunity for viruses?
Cytotoxic T cells (CD8+) - recognise viral peptide and MHC class I Cytokines with anti-viral activity - e.g. IFNγ (Class II, activate macrophages)
44
What are the 2 mechanisms of cytotoxic cells killing viruses?
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
45
What are CTLs?
Cytotoxic T lymphocytes, these act as serial killers when they recognise and bind virus-infected cells which programs death
46
What can CTLs secrete?
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
47
How do antibodies help target viruses?
Neutralise free virus - prevent spread in the body Opsonise to increase phagocytosis Activate complement leading to lysis
48
How is influenza targeted by the immune system?
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
49
How is infection of HIV controlled cytotoxic T cell response?
Patients with higher CTL activity show slower disease progression Virus mutation that escape CTL recognition may lead to progression to AIDS
50
How was knowledge of SARS-CoV-2 used to figure the immune response?
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
51
How do parasitic worms (helminths) induce immunity?
By inducing a strong IgE antibody response which allows mast cells to mediate inflammation and eosinophil antibody-dependent cell-mediated cytotoxicity
52
How is cell-mediated immunity triggered in parasites?
Protozoa survive in macrophages hidden from Igs Cytokines important in inducing macrophage activation (IL1)
53
How is T cell immunity for Leishmania mediated in mice?
BALB/c mice - fatal progressive disease C57BL/6 mice - resolve infection Differences in T cell response
54
What are the different evasion mechanisms of pathogens?
Concealment of antigens Antigenic variation Immunosuppression Interference with effector mechanisms
55
How can antigens be concealed to evade immune defence?
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)
56
What are examples of antigenic variation that evade immune defence?
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)
57
How does Streptococcus pneumoniae evade the immune system?
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
58
What are the main S.pneumoniae vaccines and how do they work?
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)
59
How does influenza evade the immune response?
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
60
What is antigenic drift?
Neutralising antibodies against haemagglutinin block binding to cells Mutations alter epitopes in haemagglutinin so that neutralising antibody no longer binds
61
What is antigenic shift?
RNA segments are exchanged between viral strains in secondary host No cross-protective immunity to virus expressing a novel haemagglutinin
62
How does Trypanosoma brucei evade the immune system?
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)
63
How does immunosuppression evade immune defence?
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)
64
What are the factors of regulatory T cells?
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
65
How does Helicobacter pylori evade the immune system?
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
66
What is regulatory T cells inducement in Leishmania?
Increase expression of T regulatory cells
67
How do measles evade the immune response?
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
68
How does the interference with effector mechanisms evade the immune system?
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
69
What are the innate pathological consequences of immune responses?
LPS induces macrophage cytokine secretion (IL1, TNFα via TLR4) Systemic effects: fever, endotoxic shock, cytokine storms
70
What are the specific pathological consequences of immune response?
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)
71
How does ebola impact the immune response?
Filovirus: enveloped, non-segmented negative stranded RNA with filamentous particles Causes haemorrhage fever Outbreak West Africa, largest in history High fatality rate (70% reported)
72
How does ebola evade the immune response?
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
73
What is the immunopathology of ebola?
Induction of cytokine storm by macrophages - central role in pathogenesis Infected macrophages express abundant tissue factor which initiates coagulation cascade - disseminated intravascular coagulation = death
74
What are examples of passive immunity?
Hypogammaglobulinaemia in infants as maternal IgG declines IVIgG very 2-4 weeks for immunodeficiency to maintain protective levels Tetnus antitoxin
75
What is active immunity?
The exploitation of immunological memory Secondary response is faster to develop and greater in magnitude and may be qualitatively better
76
What is herd immunity?
Allows immunisation of the majority of a population which protects the individual and the population (only is most are immunised)
77
What complications can occur in measles?
Ear infection - hearing loss Pneumonia - young children Sub-acute sclerosing panencephalitis (SSPE) - rare but fatal complication involving the CNS
78
When was the 1st measles vaccine introduced?
1963
79
When was the MMR vaccine introduced?
1988
80
What percentage of the population needs to be immune to prevent an outbreak?
83-94%
81
What are the requirements of an effective vaccine?
Safe High level of protection Long-lasting protection Right type of response Low cost Stable Easy to administer Minimal side effects
82
What are the different types of vaccines?
Inactivated - dead Attenuated - live but virulence disturbed Subunit - protein fragment Toxoid - bacterial toxin Conjugate - low antigenic property covalently bound to something with high
83
What are the features of inactivated vaccines?
Important antigens must survive killing May have side effects Being replaced by new vaccines
84
What are examples of attenuated vaccines?
Vaccina - smallpox Sabin - polio MMR - measles mumps and rubella BCG - tuberculosis
85
What are the pros and cons of live vaccines?
Pros: Single dose effective May be given by 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
86
What are the features of polio?
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
87
What are the features of subunit and toxoid vaccines?
Use isolated antigens Antigen is crucial May get non-responders
88
What are conjugate vaccines and name examples?
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
89
What is reverse vaccinology?
Whole genome sequencing to identify proteins that could be used as vaccines
90
What vaccine was reverse vaccinology used for?
To develop vaccine against Neisseria meningitidis group B
91
What is an example when vaccines cause the wrong type of response?
1960s vaccine respiratory syncytial virus (RSV) more serious infection suffered which lead to the death of 2 healthy children
92
What are adjuvants?
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
93
What are the different ways adjuvants work?
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
94
What is an example of adjuvants in animals and humans?
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
95
Which infections do not have effective vaccines?
Malaria Schistosomiasis Intestinal worm infestation Tuberculosis Diarrheal disease Respiratory infections HIV/AIDS
96
What is the function of the IFNγ cytokine?
Inhibit viral replication Upregulate MHC class I and II expression and antigen presentation Increase macrophage phagocytosis of dead cells Promotes NK cell killing activity
97
What species transmit leishmania?
Parasite - genus of trypanosomes Vector - sand fly
98
What does leishmania do to the immune cells?
Hide and survive in macrophages Increase expression of T regulatory cells Decrease immune response
99
What are examples of subunit and toxoid vaccines?
Hep B - surface antigen Pneumococcal polysaccharide - from capsule Tetnus toxoid - inactivated dorm of protein exotoxin secreted by bacteria

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions