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The immune system Flashcards

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1
Q

What is immunology

A

The study of the immune system,• Integrated system of cells and molecules that defends against disease and reacts against infectious pathogens

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2
Q

What are malfunctions of the immune system

A

immunodeficiency
allergy
autoimmune disease
graft rejection

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3
Q

What is the innate immune system

A

Broad specificity, not improved by repeat infection (no memory), Rapid response (hrs)

Leucocytes - Phagocytes, natural killer cells

Soluble factors - Lysozyme, complement and interferons

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4
Q

What is the adaptive immune system

A

Adaptive - Highly specific, Improved by repeat infection (memory), Slower response (days)

Leucocytes - B lymphocytes and T lymphocytes

Soluble factors - antibody

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5
Q

What are leukocytes

A

White blood cells

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6
Q

What are the 2 main lineages of WBC

A

Myeloid cells - mast cell, myoblast

lymphoid cells - Plasma cell and Natural killer cell

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7
Q

What was the first immunity to evolve

A

Innate

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8
Q

What are the external barriers to infection

A

Keratinized skin (Keratin)

Secretions (Sebum, fatty acids, lactic acid, lysozyme)

Mucous (cilia)

Low pH (stomach)

Commensals (natural bacteria)

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9
Q

What is a neutrophil

A

Main phagocyte in the blood

Short lived, fast moving

Lysosomes release enzymes (H2O2)

Faintly green

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10
Q

Where are monocytes found

A

In the blood

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11
Q

Where are macrophages found

A

In the tissues - big eater - 1 macrophage eats 100 bacteria

Long - lived

Help initiate adaptive responses

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12
Q

What does a monocyte turn into

A

Macrophage

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13
Q

What are NK cells

A

Type of lymphocyte

Kill virally infected cells non-specifically

Important in self and non self recognition

Kill cancer cells

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14
Q

What do phagocytes PRRs (pathogen-recognition receptors) recognise

A

Microbe-associated molecular patterns (MAMPs)

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15
Q

What do natural killer cells reconise

A

Kill targets unless the recognise self proteins (MHC) that are present on all nucleated cells

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16
Q

What is the complement system

A

around 20 proteins in blood which are activated on infection cause bacteria cell lysis

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17
Q

What are defensins

A
  • positively charged peptides made by neutrophils

* disrupt bacterial membranes

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18
Q

What are interferons

A

Produced by virally infected cells
• protect uninfected cells
• activate macrophages and NK cells

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19
Q

What are cytokines (interleukins)

A

hormones of the immune response
Produced by cells of the innate and adaptive immune system for cell - cell communication
Short distance

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20
Q

What are examples of inflammatory mediators

A

Histamine, prostaglandins

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21
Q

What is the integrated response to infection/injury

A

Heat
Redness
Swelling
Pain

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22
Q

What does infection/damage do to the body

A

induces the release of
INFLAMMATORY MEDIATORS (e.g. prostaglandins,
histamine) & production of CYTOKINES

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23
Q

What are the integrated responses to infection

A 
INFLAMMATION
• localised response to infection/damage
• dilation of blood vessels (redness)
• increased capillary permeability (swelling) - complement can access injury
• phagocytes migrate into tissues

TEMPERATURE
On infection, macrophages may release cytokines e.g.
interleukin 1 (IL-1)
• acts on hypothalamus
• raises temperature
• stimulates phagocytosis
• reduces level of iron in blood - less iron for bacteria growth

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24
Q

What are the 4 types of pathogen

A

Bacteria (1-5um)

Viruses (20-400nm)

Fungi (2-20um)

Parasites (1um - 10m)

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25
Q

What are features of the adaptive immunity

A

Specific

Slower

Has memory

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26
Q

What recognises the antigen

A

Receptors on T and B lymphocytes

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27
Q

Where do B cells mature

A

In Bone marrow

Receptor - Antibody

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28
Q

Where do T cells mature

A

in the Thymus

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29
Q

What does maturation do

A

Allows for the Cell receptor to form

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30
Q

What is antigen independent differentiation

A

Lymphocyte turning into a B or T cell

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31
Q

What is antigen dependent differentiation

A

A T or B cell binding to an antigen and differentiating in the lymph nodes, spleen… B cells then secrete soluble antibodies, whereas T cells kill infected host cells or make cytokines

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32
Q

What do T cells work against

What do B cells work against

A

T - Viral, intracellular bacterial and intracellular parasitic

B - extracellular bacterial, secondary viral

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33
Q

When are antibodies produced

A

In response to antigens

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34
Q

What is the clonal selection hypothesis

A

Body produces millions of different B cells each with a specific different receptor and then the B cell which can bind to the antigen undergoes clonal selection à rapid division and differentiation à clone of cells called plasma cells à secrete soluble antibody proteins

Some B cells don’t differentiate into plasma cells but instead memory cells à come across same pathogen again à divide and differentiate to destroy pathogen

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35
Q

What happens to faulty lymphocytes

A

Lymphocytes that recognise self are depleted early in development

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36
Q

What do T cells recognise

A

T cells can only recognise antigen bound to host cells

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37
Q

What do B cells recognise

A

B cells can recognise soluble antigen on the surface

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38
Q

How do T cells create an immune response

A

Millions of T cells à different T cell receptors recognise different antigen, and these T cells differentiate into T cells that can kill infected cells or produce cytokinesis à development of memory t cells

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39
Q

How is lymphoid tissue organised

A

Primary lymphoid tissue: lymphocytes reach maturity,
acquire their specific receptors (thymus and Bone marrow)

Secondary lymphoid tissue: mature lymphocytes are
stimulated by antigen

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40
Q

What is humoral immunity

A

Antigen forms B lymphocytes forms plasma cells forms a soluble antibody

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41
Q

What does humoral (antibody) immunity allow

A

Defense against extracellular bacteria and secondary

viral infections

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42
Q

What are FAB regions

A

Regions of the antibody which can bind different antigens specifically

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43
Q

What is the FC region

A

Tail of the Y

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44
Q

What does the hinge do

A

Move to antigen molecules at different distances

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45
Q

What is the dual role of immune response

A

Antigen recognition - FAB regions bind to different antigens specifically
Antigen elimination - Fc region binds to complement, Fc receptors on phagocytes

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46
Q

What is the structure of an antibody

A

Light chain - 25kD
Heavy chain - 50kD
Immunoglobulin G = L2H2 = 150kD
Immunoglobulin domain

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47
Q

What does papain do

A

Cleaves the molecules and gives two fragments - FAB and FC

FAB - Fragment antigen binding
FC - Fragment crystallizable

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48
Q

What is the ratio of FAB to Fc

A

2:1

49
Q

What is the variable and constant regions

A

Variable regions – bind antigens. Differ between antigens with different specificities

Constant regions – same for antibodies of a given H or L chain type

50
Q

How can V region exons create different antibody specificities

A

RECOMBINE and MUTATE

during B cell differentiation

51
Q

What are the different classes of immunoglobulin

A

IgG y - main class in serum and tissues, important in secondary/memory responses crosses the placenta
IgM u - Important in primary response
IgA a - In serum and secretions protects muscosal surfaces
IgD d - Unknown
IgE e - Present at very low levels, protective against parasites, involved in allergy

52
Q

What are the 2 types of light chain

A

Kappa and lambda. Not class restrictive. Can have IgGk or IgG lambda

53
Q

How many antigens can bind to IgA and IgM

A

IgA is secreted as a dimer so can bind to 4 antigens at once

IgM is a pentamer in serum – Can bind to 10 antigens at once

54
Q

When is IgM used (primary or secondary)

A

IgM is more used in primary response as it can bind 5 different antigens so more likely to bind to pathogens whereas IgG is used in secondary response as it is highly specific

55
Q

What is serum

A

blood which has been allowed to clot. Clear fluid

56
Q

What antibodies are used in secondary response

A

IgG (and other classes)

57
Q

How do the immunoglobulins differ

A

Five classes of immunoglobulins differ in the amino acid sequence of their heavy chains

58
Q

What are antibodies made of

A

made up of two longer (heavy) chains and two smaller (light)

chains, each made up of compact, globular domains.

59
Q

How do antibodies protect against infection

A 
Specific binding proteins (FAB)
Neutralise toxins (IgG, IgA)

Immobilise – motile microbes (IgM)

Prevent binding to and infection of host cells

Form complexes

Effector functions (Fc)

Effect removal and destruction of pathogen

Activate complement - (IgG, IgM)

Bind Fc receptors
Phagocytes - (IgG, IgA)
Mast cells - (IgE)
Natural killer cells - (IgG) `

60
Q

What does complement do

A

Complements the activity of antibodies in destroying bacterial cells

Induces inflammation

Beneficial in the early stages of an immune response

61
Q

How is complement activated

A

20 serum proteins are activated via an enzyme cascade

Activated specifically by antigen/antibody complexes
(CLASSICAL pathway) or non-specifically by e.g. certain
bacteria (MB-LECTIN or ALTERNATIVE pathway).

62
Q

What are the main components of the classical complement pathway

A

C1-9

C3 is the most abundant

63
Q

What is the classical complement pathway

A

Classical requires 1xantigen and 2xantibodies

Complement 1,2,4 binds to Fc region

2 of the heads need to be bound to activate complement

Why IgM is more potent activator of complement as it’s a pentamer

Activation of C1, C4 and C2 leads to the generation of a C3 convertase

C3b joins the C3 convertase to make a C5 convertase

64
Q

What are the main biological activities of complement

A

Activation - C5a, chemoattractant, anaphylatoxins, bind to mast cells which become activated and release histamine ,released in response to anaphylatoxins

Opsonization - C3b, increased binding and phagocytosis - “makes tasty”, Coats bacteria

Cell lysis - membrane attack complex - C5 - 9 –> hollow cylinders which form pores in bacterial membranes

65
Q

What type of bacteria are not susceptible to membrane attack complex

A

Gram-positive

66
Q

What types of antibodies can act as opsonins

A

IgG and IgA

67
Q

How do antibodies enhance the recognition of microbes

A

binding to Fc receptors on the phagocyte surface.

68
Q

How do phagocytes kill bacteria

A

Phagocytes create pseudopods to encapsulate bacteria –> Pseudopods fuse → phagosome → lyzosomes fuse with phagosome → phagolysosome –> bacteria killed

69
Q

How do Fc receptors on NK cells cause apoptosis

A

Secrete perforin –> like complement membrane attack complex

NK uses perforin channel to secrete enzymes into target

Activates apoptotic pathway so target cell commits suicide

Mediated by IgG

70
Q

What do mast cells do

A

Mediate allergy and defence against large parasites – bind with very high affinity for Fc regions of IgE

71
Q

Where are mast cells found

A

Under mucosal layer

72
Q

How can antibodies be used in medicine

A

Producing antisera

73
Q

What do polyclonal B cells respond to

A

Antigen

May lack fine specificity
Difficult to standardise

74
Q

What is the epitope

A

The shape of antigen

75
Q

How are monoclonal antibodies made

A

B cells from animal immunised with Antigen A + tumour cell line fused together.

Cell now divides indefinitely and makes antibody A

76
Q

What are humansied antibodies

A

antibodies from non-human species whose protein sequences have been modified to increase their similarity to antibody variants produced naturally in humans.

77
Q

What are the 2 main subpopulations of T lymphocytes

A

T helper cells - CD4+ve

T cytotoxic cell - CD8+ve - 33% of T cells

78
Q

What do Th cells do

A

Help B cells make antibody
Activate macrophages and natural killer cells
Help development of cytotoxic T cells

Cytokines

79
Q

What do T cytotoxic cells do

A

Recognise and kill infected host cells

80
Q

What is the TCR

A

The T cell receptor is very similar to the Fab arm of an antibody

Important in recognizing fragments of antigen as peptides bound to major histocompatibility complex (MHC) molecules.

81
Q

How do T cells recognise antigen

A

B cells recognise soluble free native antigens

T cells recognise cell associated processed antigen

82
Q

Where is the MHC found

A

Chromosome 6

83
Q

What is the MHC for

A

Important in graft rejection

Very polymorphic

Major role in initiating T cell response

84
Q

Where are MHCs found

A

Red blood cells don’t have MHC proteins

Organs do

85
Q

What is MHC 1

A

Expressed by all nucleated cells – not RBC

Display antigen cytotoxic (CD8+ve) T cells

86
Q

What is MHC 2

A

expressed by macrophages, dendritic cells, B cells

display antigen to CD4+ve (helper) T cells

87
Q

What does cytotoxic T cell recognise

A

peptide bound to MHCI

88
Q

How do cytoxic T cells become activated

A

Cytotoxic T cell recognises peptide bound to MHC1

Virus-infected cell creates viral proteins, broken down in cytosol (proteosomes)

Peptides transported to ER, bind MHC1 at cell surface

Activated cytotoxic T cells kill the infected cell (perforins) by inducing apoptosis

89
Q

How do T helper cells become activated

A

Helper T cell recognise peptide bound to MHCII

Macrophage/dendritic cell/B cell internalise and breaks down foreign material

Peptides bind to MHC II in endosomes à cell surface

Activated T helper cells help B cells make antibody, produce cytokines that activate and regulate other leucocytes

90
Q

What is thymic selection

A

T cells acquire their receptors and are educated in the thymus

Only T cells that recognise self MHC, but not self-peptides survive

91
Q

How many T cells go to peripheral lymphoid tissue

A

5%

92
Q

What are cytokines

A

Hormones of the immune response
Small (5-20kD) secreted proteins involved in communication between cells of the immune response

Usually produced and act locally

Bind to specific receptors which are present on target cell

93
Q

What are the main groups of cytokines

A

Interleukins (IL-1, IL-38?) – usually made by T cells
Interferons (IFNs) - viral infections e.g. IFNα, IFNβ; cell
activation (IFN γ)
Chemokines - cell movement or chemotaxis e.g. IL-8
Colony stimulating factors (CSFs) – leukocyte production
e.g. GM-CSF

94
Q

What does the binding of a cytokine do

A

causes cell activation and changes in gene expression

95
Q

What is an overview of the adaptive immune response

LONG LONG LONG LONG ANSWER HEHEHEHE

A

Infection caused by bacteria –> macrophages and dendritic cells recognise the infection –> enter the nearest lymph node from infected site –> macrophages and dendritic carry foreign material through lymphatics into the lymph node –> naïve T cells in lymph (haven’t seen antigens before)–> divide and differentiate via clonal selection –> macrophages and dendritic cells activate T cells which dive into Tk or Th cells –> Th cells can help B cells differentiae into plasma cells and secrete antibody –> b cells stay in lymph node –> T effector cells leave the lymph node and go to where they’re needed in the tissues

96
Q

Who invented the vacine

A

Edward Jenner

97
Q

What are the types of vaccine

A 
Attenuated strains
Killed pathogen
Subunit e.g. toxoid (derived from toxin)
Vaccination
Engineered virus, RNA, DNA
98
Q

When was aids first recognised

A

1981

99
Q

When was HIV identified

A

1983

100
Q

What is HIV (type of virus)

A

Retrovirus - has reverse transcrptase - Allows RNA to turn into DNA which enters host cell chromosome

Lentivirus - Slow virus - cause disease long time after infection

101
Q

What is the lifecycle of HIV

A

Virus binds to cell receptor
Virus envelope fuses with plasma membrane
Nucleocapsid enters cytoplasm
Viral RNA reverse transcribed into double stranded DNA
Viral DNA transported to nucleus and integrates into host cell genome (provirus)
New viral genomic RNA and mRNA → cytoplasm
Viral mRNA → viral protein
New nucleocapsids forms and virus “buds” from cell, acquiring
lipid envelope

102
Q

What are the types of retroviral infection

A

Latent - no virus shedding
Permissive - few particles, host cell doesnt die
Lytic - lots of virus particles –> kills host cell

103
Q

What cell type is susceptible to HIV

A

CD4+ve (Th cell, Monocytes, macrophages and dendritic cells)

104
Q

What happens to number of T cells through each round of replication

A

Increases with each round of

viral replication

105
Q

What is needed for HIV infection

A

CD4 and Co-receptor - CCR5 required for virus fusion with host cell

106
Q

How does the CNS become involved in HIV

A

Monocytes may traverse the blood/brain barrier → CNS

involvement

107
Q

What causes AIDS

A

Th cell depletion

Direct lysis by virus, syncytium formation
Killed by cytotoxic T cells or other immune mechanisms

Apoptosis

Blood count CD4+veTcells < 200/mm^3

108
Q

Where are infected Th cells

A

Lymphoid tissue (PCR discovered)

109
Q

`What are symptoms associated with AIDS

A

Susceptible to pathogens that healthy people would fight off

o Opportunistic infections

o Reactivation of latent viruses

o Rare cancers

o CNS involvement, dementia

o Memory T cells lost

o All adaptive immune responses are compromised

110
Q

Where did HIV-1 originate

A

Central Africa

Group M –> pandemic form

Related virus affecting subgroup of chimpanzees

Phylogenetic studies suggest cross-species
transmission 1910 – 1930

111
Q

Where did HIV 2 originate

A

Origin West Africa

Pre-dates HIV-1.

Likely source - related virus
affecting sooty mangabees

Less virulent and less easily
transmitted

112
Q

How many people are infected with HIV (2019)

A

38million

Total >70million with 33 million dead

113
Q

How is HIV spread

A

unprotected sexual intercourse (~70%)
• blood/blood products (~28%, mainly i.v. drug use)
• breast-feeding
• mother to foetus

114
Q

What are the prevention and therapy methods

A

blood testing
“safe sex”
decrease i.v. drug use/needle sharing
treat HIV+ve pregnant women

This is decreasing HIV by around 1million in last 10 years

115
Q

Why is there no vaccine for HIV

A

high mutation rate of virus - 60x more rapid mutations than flu

  • “humoral” immunity may not be protective
  • need to induce cytotoxic T cells
116
Q

What are the problems of drug therapy

A
  • high mutation rate of virus
  • toxicity
  • viral latency
  • cost

> 25 licensed drugs block HIV replication

117
Q

What is combination therapy

A
  • cocktail of drugs directed at different viral targets
118
Q

What are the future treatments of HIV

A

Stem cell therapy (bone marrow cells lacking CCR5)

Immunisation of infected patients: “Kick and Kill”

“Passive immunisation” using human monoclonal antibodies or engineered T cells

Gene editing with CRISPR/Cas9?

University - Microbiology (8 decks)

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