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POM Revision Cards > Immunology > Flashcards

Immunology Flashcards

1
Q

Protonsil?

A

First sulphonamide, bacteriostatic, gram positive bacteria.
UTIs, RTIs, bacteraemia, prophylaxis for HIV.

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2
Q

Beta-lactams?

A

Interfere with synthesis of peptidoglycan component of bacterial cell wall.
Penicillin, methicillin.
Bind to penicillin binding proteins which usually catalyse steps in synthesis of peptidoglycan.

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3
Q

Aminoglycosides?

A

E.g. gentamicin, streptomycin.
Bactericidal.
Target protein synthesis (30S ribosomal subunit), damages cell membrane.

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4
Q

Rifampicin?

A

Bactericidal, targets RpoB subunit of RNA polymerase.
Spontaneous resistance frequent.
Secretions go red/orange.

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5
Q

Vancomycin?

A

Bactericidal.
Targets lipid II component of cell wall biosynthesis and wall cross linking (via D-ala residues).

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6
Q

Linezolid?

A

Bacteriostatic, inhibits initiation of protein synthesis by binding 50S rRNA subunit.
Gram positive.

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7
Q

Daptomycin?

A

Bactericidal.
Targets cell membrane.
Gram positive.

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8
Q

Macrolides?

A

E.g. erythromycin, azithromycin.
Gram positive, some gram negative.
Target 50S ribosomal subunit, prevents amino-acyl transfer + truncation of polypeptides.

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9
Q

Quinolones?

A

Synthetic broad spectrum, bactericidal.
Targets DNA girase in gram negative, and topoisomerase IV in gram positive.

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10
Q

Antibiotic resistance mechanisms?

A

Altered target site
Inactivation of antibiotic
Metabolism altered
Decreased drug accumulation

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11
Q

Sources of antibiotic resistance?

A

Plasmids
Transposons
Naked DNA

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12
Q

Mechanisms for horizontal spread of AB resistance?

A

Transformation - uptake of extracellular DNA
Conjugation - phage-mediated DNA transfer
Transduction - pilis-mediated DNA transfer

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13
Q

Non-genetic mechanisms for AB resistance?

A

Biofilm
Intracellular location
Slow growth
Spores
Persisters

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14
Q

Ways of avoiding opsonisation?

A

Expression of capsule polysaccharide - both SA and SP

Surface proteins bind Fc region - S. aureus = protein A, S. pyogenes = protein M.

Proteases degrade antibodies - S. pyogenes only, cleaves antibodies using IdeS.

Antigenic variation - Opa + LOS antigens on N. gonorrhoeae.

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15
Q

Steps in complement cascade?

A
  1. Initiation
  2. Formation of C3 convertase
  3. Formation of C5 convertase
  4. MAC formation
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16
Q

Ways of evading complement?

A

Degrade C3 - prevents C3b deposition and C3a and C5a formation. S. aureus uses Aur, S. pyogenes uses SpeB.

Inhibit C3 or C5 convertases - prevents C3a and C5a formation and C3b deposition. S. aureus uses SCIN protein to bind to C3bBb.

Recruit negative regulators - S. aureus recruits factor H, S. pyogenes recruits factor H and C4BP.

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17
Q

Different neutrophil PRRs?

A

TLR - detect conserved microbial structures
CLEC - detect microbial carbohydrates
FPR - detect formylated peptides.

also use Fc or complement receptors for opsonised microbes, or cytokine and chemoattractant receptors for chemotaxis

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18
Q

Ways that bacteria evades neutrophils?

A

Inhibit chemotaxis - S. aureus uses CHIPs to bind C5aR, S. pyogenes uses SpyCEP to cleave CXCL8 so CXCR1/2 cannot bind.

Inhibit phagocytosis - S. aureus uses FLIPr + SSL5 to block Fc receptors.

Kill neutrophils - using toxins

Disrupt intracellular signalling.

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19
Q

FLIPr + SSL5?

A

S. aureus, inhibit neutrophil phagocytosis.
FLIPr - Fc gamma, IgG inhibitors.
SSL5 - Fc alpha, IgA inhibitors.

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20
Q

Virus examples of escaping AB recognition?

A

Rhinovirus - exists as hundreds of antigenetically distinct serotypes
HIV - exist as multiple clades or quasi-species
Hep B + Ebola - encode secreted surface antigens that mop up antibodies
Dengue virus - exists as 4 serotypes
Influenza - antigenic drift + shift

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21
Q

Interferons?

A

Initiate antiviral state - transcription of genes that block viral replication (2’5’oligoadenylate synthetase and protein kinase R).

Type I - IFN alpha (with IL-12, activate NK cells) and beta.
Type II - IFN gamma, produced by activated T cells and NK cells
Type III - IFN lambda

hep B and influenza can inhibit IFN transcription

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22
Q

Viral life cycle?

A
  1. Attachment
  2. Insertion
  3. Translation (using host cell ribosomes and machinery)
  4. Assembly
  5. Exocytosis (budding or cytolysis)
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23
Q

Viral detection?

A

Viral genome - PCR
Viral antigen - ELISA
Viral particles - electron microscope
Cytopathic effect - isolation and culture
Anti-viral antibodies - serology

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24
Q

Amantadine?

A

Antiviral for Influenza A.
Blocks M2 ion channel so virus is locked inside endosome due to no H+ entry, prevents uncoating.
Most H3N2 viruses are resistant.

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25
Q

Neuraminidase inhibitors?

A

For influenza.
Tamiflu - inhibits NA enzyme that cleaves sialic acid so prevents spread of new virus particles.
Relenza - viruses more readily acquire resistance so not as effective as Tamiflu.

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26
Q

Acyclovir?

A

For herpes (HSV-1), resistance rare.
Prevents phosphodiester bond. Nucleoside analogue.
Needs thymidine kinase for ACV->ACVMP->ACVTP, so very specific as only activated inside of virus infected cells.

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27
Q

Remdesivir?

A

For Hep C.
Analogue of adenosine, causes chain termination 3 nucleotides downstream.

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28
Q

HIV treatments?

A

HAART, PrEP, AZT.
Aim to inhibit entry, fusion, reverse transcriptase, integrase or proteases.

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29
Q

HIV life cycle?

A
  1. Binds to CD4 using gp120 then enters cell
  2. Reverse transcriptase causes RNA -> DNA, incorporated into host cell DNA using integrase.
  3. Production of RNA + proteins
  4. Budding to release virion.
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30
Q

Influenza life cycle?

A
  1. Attachment - haemagglutinin spike protein binds to virus receptor and entry via endocytosis
  2. Capsid falls, exposes RNA negative sense genomes
  3. mRNA made using RNA-dependent RNA polymerase.
  4. Cytolytic release using Neuraminidase.
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31
Q

Response to intracellular pathogens (bacteria and Protozoa)?

A

Macrophages activated, release IFN gamma, T cell activated and differentiate into Th1.

32
Q

Response to Helminiths, allergens and venom?

A

Mast cells and oesinophils activates, release IL-4, 5 and 13, T cell activated, differentiate into Th2.

33
Q

Response to extracellular bacteria and fungi?

A

Neutrophils activated, release IL-17 + 22, T cell activated, differentiate into Th17.

34
Q

AIRE?

A

Autoimmune regulator, transcription factor, promotes self-tolerance by presenting genes usually expressed in peripheral tissues to T cells whilst in thymus. Allows T cells to encounter MHC bearing peptides usually expressed in other body parts.
Autoimmune Polyendocrinopathy syndrome type 1 - mutation in AIRE.

35
Q

Importance of B cell peripheral tolerance?

A

Due to somatic hypermutation (affinity maturation) in which B cells change specificity after leaving bone marrow to generate antibody diversity. Usually good but can cause autoimmunity.
E.g anti-streptococcus pyogenes can cross react with heart muscle as antigens similar.

36
Q

Mechanisms for T cell peripheral tolerance?

A

Anergy - if naive T cell sees MHC/peptide ligand without co-stimulatory protein, becomes anergic (less likely to be stimulated in future).
Ignorance - T cells separated from antigens or too low concentration for protection if self reactive. Compartmentalisation of cells in immunologically privileged sites (eyes, brain).
Antigen induced cell death - APCs promote apoptosis through death ligand - Fas ligand, FasL/CD95 ligand.

37
Q

Treg?

A

Inhibit other T cells by secreting immune-suppressive cytokines (TGF beta, IL-10, IL-35) and inactivate DC.
CD4, IL-2 receptor (CD25), Foxp3 (helps Treg mature) transcription factors - markers of Treg cells.
Mutation in Foxp3 - IPEX syndrome.

38
Q

IL-10?

A

Anti-inflammatory, blocks pro-inflammatory cytokine synthesis (TNF, IL-6, IL-8, IFNgamma), downregulates macrophage activity, plaiotrophic.
Viruses can mimic sometimes to escape immune system.

39
Q

nTreg and iTreg?

A

nTreg - develop in thymus, require recognition of self antigen, reside in peripheral tissue to prevent harmful reactions to self.

iTreg - develop during T immune response from CD4 T cells, to prevent collateral damage.

40
Q

Tfh and B cell communication?

A

Expresses CD40L, activates B cells which expresses B7. B7 activates T cells on CD28 which then releases cytokines (IL-21).

41
Q

T cells boost B cells?

A

CD4 release cytokines, detected by B cell which alters its constant region to determine Ig class switches.

42
Q

Type 1 hypersensitivity?

A

IgE mediated, immediate/anaphylactic.

  1. Sensitisation
  2. Th2 cells and Tfh cells produce IL-4 and 13.
  3. Causes B cells to class switch from IgM to IgE.
  4. Th2 recruit eosinophils
  5. Mast cells and basophils degranulate after cross linking.
43
Q

Type 2 hypersensitivity?

A

Antibody mediated cytotoxic hypersensitivity. Destruction of IgG or IgM antibodies bound to antigens present on surface of cells.
E.g immune thrombocytopenia, mismatched blood transfusion, Graves.
1. Anti-receptor activity - blocking or activating its function.
2. Antibody-dependent cell-mediated cytotoxicity
3. Classical activation of complement cascade.

44
Q

Type 3 hypersensitivity?

A

Immune complex driven disease. Immune complexes cannot be cleared so accumulate and are deposited in blood vessel wall, causing IgM -> IgG.
E.g systemic lupus erythomatosus - IgGs against DNA or proteins in nucleus. Forms persistent immune complex deposits.
Also multiple sclerosis and rheumatoid arthritis (autoimmune).

45
Q

Type 4 hypersensitivity?

A

T cell mediated, delayed type. Only hypersensitivity that isn’t antibody mediated.
2 phases:
1. Sensitisation
2. Re exposure
E.g contact dermatitis (urushiol acts as a hapten)

46
Q

Th cells?

A

Tfh - pro-antibody, IL-21, support B cells
Th1 - pro-inflammatory, boosts cellular immune response, IFN-gamma, TNF, IL-12.
Th2 - pro-allergic (and worms), boosts multicellular response, IL-4, 5 and 13.
Th17 - pro-inflammatory, control bacterial and fungal infection, IL-17, 23, 6 and neutrophils.
Treg - anti-inflammatory, limits immune response, IL-10, TGF beta.

47
Q

Interleukins functions and which Th cell produced by?

A

1 - fever, Th1
2 - T cell stimulation, Th1
3 - bone marrow stimulation (and myeloid progenitor cells), Th1
4 - class switching to IgE, Th2
5 - IgA, eosinophils, promote antibody production, Th2
6 - acute phase protein production and fever, Th17
8 - neutrophil chemotaxis
10 - anti-inflammatory, Treg
12 - differentiation of CD4 T cells into Th1

48
Q

IFN gamma and TNF alpha?

A

IFN gamma - activates macrophages, produced by Th1.

TNF alpha - cytotoxic to tumour cells, pro-inflammatory, produced by Th1.

49
Q

Apoptosis by CD8?

A

Contain perforin, granzymes and granulysin.
Perforin polymerise, form pores. Granzymes then injected into cell.

50
Q

Antibody classes?

A

IgG - highest neutralisation and opsonisation activities, 4 subtypes.
IgM - produced first upon antigen invasion, pentameric shape, increases transiently.
IgA - expressed in mucosal tissues, forms dimmers after secretion.
IgD
IgE - involved in allergy.

51
Q

Thymus independent vs dependent? (Accessory signals)

A

Independent - without help of T cells. Often polysaccharide (LPS), second signal requires provided by PAMPs (LPS). Only IgM, no memory.
Dependent - BCR recognises antigen and internalises it, degrades it into peptides. Peptides associated with ‘self’ molecules (MHC II) and expressed on surface. Recognised by CD4 Th cell, and B cell activated. Class switched.

52
Q

What is in a vaccine?

A

Antigen, adjuvant (usually alum), stabilising stuff (buffy coat) and water.

adjuvants activate dendritic cells to present antigen to T cells, part of licensing response. Upregulates stimulatory signalling and cytokines. E.g AS03, MF59, alum

53
Q

Different types of vaccines with examples?

A

Inactivated toxoid vaccines - tetanus toxoid
Recombinant protein vaccines - Hep B surface antigen
Conjugate vaccines - S. pneumoniae
Dead pathogen - influenza split vaccine
Live attenuated vaccines - BCG, LAIV, OPV.

54
Q

Baloxavir

A

decrease virus shedding, interrupting transmission

55
Q

Gram stains?

A
  1. Crystal violet
  2. Lugol’s iodine
  3. Alcohol (dehydrates peptidoglycan area, makes it tighter)
  4. Safranin

positive, 1 thick peptidoglycan cell wall = purple

negative, 2 outer membranes with thin peptidoglycan component between = pink

56
Q

Components of PCR?

A
  • DNA template
  • Primers (forward and reverse) - bind to tax gene and amplify the 300 bp region
  • DNA polymerase (often Taq polymerase) - extends the DNA strands
  • dNTPs (deoxynucleotides) - building blocks do DNA
  • Reaction buffer - provides appropriate salt and pH environment for polymerase to work
57
Q

PCR steps?

A
  1. Denaturation - 1 minute at 95 degrees to denature dsDNA to produce ssDNA
  2. Annealing - sample cooled to 54 degrees for 45 seconds to allow forward and reverse primers to anneal to DNA with complementary sequence.
  3. Extension - sample heated to 72 degrees for 2 minutes which is optimal temperature for thermos table DNA polymerase to extend DNA and produce second strand. (Only dNTPs)

repeated 30-40 times

58
Q

How are PCR DNA samples analysed?

A

DNA gel electrophoresis - DNA is negatively charges and migrates to positive electrode. DNA visualised with intercalating DNA stain.

DNA loading dye increases weight of DNA, shows wells, and indicates how far DNA fragments have migrated during run
DNA marker ladder estimates the size of the PCR fragment

59
Q

qRT-PCR?

A

Shows severity of the disease and likelihood of transmission rather than only yes/no (like in regular PCR).
Very similar to PCR but instead of electrophoresis, amount of PCR is monitored throughout reaction cycle.
an increase in fluorescent signal is proportional to amount of DNA in sample. Low CT value = high load and vice versa
Expensive.

60
Q

2 common methods of doing qPCR?

A
  1. Fluorescence dye-based method
  2. DNA probe-based method (TaqMan) - third oligoprobe added to mixture which binds to specific gene that’ll be amplified in region between forward and reverse primers. Oligoprobe with fluoroscope attached at 5’ end and a quencher attached on 3’ end.
61
Q

Gram stain steps?

A
  1. Crystal violet - bacterial cell walls retain
  2. Iodine - forms crystal violet-iodine complex
  3. Alcohol - dehydrates peptidoglycan area, becomes tighter
  4. Safranin - decolourises gram-negative bacteria

gram negative = pink, gram positive = purple

62
Q

Gram positive vs gram negative?

A

Positive = 1 outer membrane with thick peptidoglycan around it
Negative = 2 outer membranes with thin peptidoglycan layer in middle, along with lipopolysaccharide layer. Cell wall made of peptidoglycan.

63
Q

Catalase test?

A

Test if bacteria can produce catalase which catalyses breakdown of hydrogen peroxide into H2 and O2.
Positive = bubbles, staphylococci.
Negative = no bubbles, streptococci.

64
Q

Haemolysis test?

A

For streptococci, tests capacity of bacteria to produce haemolysins.
Alpha - partial haemolysis (S pneumoniae)
Beta - complete haemolysis (S pyogenes)
Gamma - no haemolysis (S faecium)

65
Q

Coagulase test?

A

For staphylococcus, tests if bacteria can produce coagulase (enzyme that cross-links fibrinogen to produce a clot on bacterial surface)
Positive = clumps (S aureus)
Negative = no clumps (S epidermidis)

66
Q

Lactose fermentation?

A

For gram-negative Bacilli, tests capacity of bacteria to ferment lactose to lactic acid (so contain lactase)
Lactose-fermenter - Agar shows pink colonies after being incubated overnight (E coli, K pneumoniae)
Lactose non-fermenter - colourless (yellow colonies) on Agar plate. (Salmonella)

67
Q

Minimum inhibitory concentration and selective toxicity

A

MIC - minimum concentration to inhibit growth

Selective toxicity - toxic to pathogen but not human cells

68
Q

Ribosome target antibiotics?

A

Aminoglycosides
Linezolid
Macrolides

69
Q

Cell wall/membrane target antibiotics?

A

Beta lactams - wall
Vancomycin - lipid II wall
Daptomycin - membrane

70
Q

Passive immunotherapy?

A

Antibodies from recovered individuals or produced in the lab from immortalised B cells

71
Q

ROS and NO

A

Released by effector mechanisms to kill microbes

72
Q

Soluble effector mechanisms?

A

Complement mediated
Lectin-binding
Iron chelation
Antibiotic-like peptides

73
Q

3 signals for T cell activation?

A

Antigen recognition
Co-stimulation
Cytokine release

74
Q

When is apoptosis triggered in B cells?

A

If immature B cells encounter antigen in a form which can cross link their IgM.

75
Q

Conjugate vaccine?

A

Polysaccharide coat component is coupled to immunogenic carrier protein

POM Revision Cards (7 decks)

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