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Immunity To Infection Flashcards

1
Q

What are commensals?

A

A micro organism that lives continuously in the body without causing disease

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2
Q

When do opportunistic pathogens cause disease

A

Only when host defence is compromised

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3
Q

What percentage of human genes are involved in defence

A

10%

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4
Q

Do innate immunity responses vary with the type of micro organism

A

Yes

The nature of pathogen is recognised and this information is passed on to the adaptive system

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5
Q

Does the adaptive immune system use the innate immune system

A

Adaptive responses co-opt many of the effective mechanisms of the innate system in a highly specific way to deal with infection

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6
Q

What kind of response is inflammation

What is its purpose

A

A stereotypic response to tissue injury, which can be sterile

To eliminate the initial cause of cell injury, remove damage/necrotic tissue resulting from injury or the subsequent immune response and to initiate repair of the damaged tissue

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7
Q

How is localised acute inflammation classically recognised

What causes each

A

Calour (heat) - increases blood flow
Dolor (pain) - stimulation of nerve endings
Rubor (redness) - increased circulation/ vasodilation
Tumor (swelling) - increased fluid in tissues

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8
Q

What are the two important features of epithelial barriers in the immune system

A

Physical

Secretions

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9
Q

What are the three key components of the immune system

A

Epithelial barriers

Cellular barriers

Soluble components

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10
Q

Describe the immune function of the physical epithelial barrier

A

TEpithelial barriers separate the host tissue from external environment

Tight junctions between squamous epithelial cells of the skin and mucosal glandular epithelium of the GI and respiratory tract prevent access to tissues

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11
Q

Describe the immune function of secretions from epithelial barriers (4)

A

Mucus covers all glandular surface

Stomach acid

Antimicrobial peptides which damage microbial membranes

Enzymes in tears and saliva (lysozyme,) or stomach (pepsin)

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12
Q

Where are white blood cells generated in adults

A

In the bone marrow by a process called haematopoiesis

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13
Q

What gives rise to B, T and Natural Killer cells

A

The lymphoid lineage

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14
Q

What does the common myeloid progenitor give rise to (6)

A

The 3 granulocytes

Mast cells

Circulating monocytes

Dendritic cells

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15
Q

What are the granulocytes

A

Neutrophil

Basophil

Eosinophil

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16
Q

Which is the most abundant white blood cell

A

Neutrophil

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17
Q

Where do neutrophils mobilise to

What guides neutrophils

A

Sites of infection

C5a and fMLF

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18
Q

What is the life span of a neutrophil

A

Very short lived

They mobilise to the site of infection, phagocytose the microbe and then die

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19
Q

What happens to neutrophils after death

A

They degranulate, releasing antibacterial proteins into the ECF

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20
Q

What is a NET and how is it made

A

Neutrophil extracellular trap
They trap microbes (PUS)

made when neutrophils extrude their DNA

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21
Q

What do macrophages do

A

They are large phagocytic cells that recognise and engulf microbes and dispose of cell debris

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22
Q

What are the two effector sunsets of macrophages

A

M1 and M2

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23
Q

What do M1 macrophages do

A

Secrete cytokines and pro inflammatory mediators that stimulate the acute inflammatory response

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24
Q

How do M2 macrophages work

A

AKA alternatively activated macrophages

They are associated with tissue repair and parasite killing and explosion

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25
Q

What do mast cells contain

What is their overall function

A

Pre-formed mediators of inflammation such as histamine

To rapidly induce inflammation

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26
Q

How long do mast cells take to degranulate once activated

What causes mast cell degranulation?

A

Only Seconds

Allergens (IgE)
PAMPs and DAMPS
Complement components (C3a, C5a)
Substance P (neurogenic inflammation)

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27
Q

Where do both mast cells and macrophages reside

A

Beneath epithelial surfaces where they function as sentinel cells sensing tissue damage

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28
Q

Give a brief description of the function of eosinophils and basophils

A

Non-phagocytic granulocytes providing defence against hemliths, worms and other parasites

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29
Q

What do you dendritic cells function as

A

A bridge between innate and adaptive systems

They Recognise pathogen is at the site of infection in the periphery and carry a record of the encounter to the draining lymph-node’s to initiate the adaptive response

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30
Q

What are the three major players in the innate system

A

NK cells
Phagocytes
Complement

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31
Q

What do natural killer cells do

A

They moved to circulate in the blood in a partially activated state ready to respond immediately

They move into infected tissue and proliferate

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32
Q

What are NK cells v important for

A

are very important in viral infections where they kill infected cells and maintain/increase the state of the information of infected tissue

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33
Q

What are the two broad ways NK cells recognise infection

A

Missing self (loss of molecules that normal cells express)

Induced self (Expression of self molecules that are induced in stress cells)

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34
Q

What does NK cell response depend on

A

The balance of signalling derived from activating and inhibitory responses

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35
Q

Which NK receptors dominate in healthy cells

A

Inhibitory receptors

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36
Q

Where does a major inhibitory signal come from on healthy cells

A

Recognition of Major Histocompatibility Complex (MHC) class 1 molecules

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37
Q

How do MHC Class 1 molecules work

A

They present peptide fragments, derived from cytosolic pathogens (e.g. viruses) to T cells, signalling the virus-infected cells should be killed

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38
Q

How have viruses evolved mechanisms to escape T-cells

How do we combat this

A

They have removed MHC class 1 molecules so fragments from the virus can not be presented to the T cells

NK cells can recognise a lack of MHC as “missing self” and killing is activated

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39
Q

What is induced self

A

When cells are infected/stressed, they respond by expressing cell-surface ligands for NK activating receptors, pushing the signalling balance towards activation

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40
Q

What do they cytokines (type 1 IFNs) produced by viruses cause in the host’s immune system

A

Induced resistance in surrounding cells (anti-viral state)

Increase in expression of ligands recognised by indicate receptors

Activate NK cells to kill

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41
Q

Which cytokines do local macrophages produce

What do these cytokines do

A

CXCL8
IL-12

They recruit and activate NK cells and cause their proliferation

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42
Q

Do NK cells produce cytokines

What do these do

A

Yes (IFNγ)

Activate macrophages and up regulate killing capacity

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43
Q

3 effector functions of NK cells

A

1) release perforin
2) ADCC
3) macrophage activation

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44
Q

What does perforin do

A

Released by NK cells and Forms pores in the cell membrane allowing apoptotic granzymes into the cell

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45
Q

Describe ADCC

A

Antibody Dependant Cell Cytotoxicity

NK cells have receptors for the Fc portion of antibodies and will kill cells that are bound by that antibody

Signalling through this activating Fc receptor is very strong and is enough to activate Nk cell by itself

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46
Q

Innate Lymphoid Cells are similar to which group of T cells

A

CD8 cytotoxic T lymphocytes (CTLs)

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47
Q

What do ICLs do

A

The ILCs help orchestrate the early innate response

They derive from the common lymphoid progenitor but do not possess B or T cell antigen receptors

They do not directly control infection (like NK cells) but instead function to amplify signals produced during innate recognition

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48
Q

What are the three major types of ILCs

A

ILC1s
ILC2s
ILC3s

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49
Q

What do ILC1s

A

They protect against viruses and intracellular pathogen is

They help activate M1 macrophage responses and may assist TH1 polarisation

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50
Q

What do ILC2s do

A

Assist mucosal and barrier immunity against parasites

They indirectly help TH2 and M2 macrophage polarisation

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51
Q

What do ILC3s do

A

Protect against extracellular bacteria and fungi

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52
Q

What are cytokines

What is their life span

A

Small protein messengers which regulate immune responses

Short lived

53
Q

True or false

Cytokine action is autocrine

A

True but it can also be paracrine and endocrine-like

54
Q

Give for traits of cytokines

A

Redundancy
Pleiotropism
Antagonism
Synergy

55
Q

What is redundancy in cytokines

What about antagonism

Pleiotropism

A

Several different cytokines have the same function

1 cytokine May block the action of another

A single cytokine may have a variety of different effects

56
Q

Name a central communication system for the immune system

Name a type of molecule that works through this pathway

A

Jak/ STAT signal transduction pathway

Cytokines

57
Q

What was IL-8 renamed

It is a member of which subgroup of cytokines? What is this subgroup involved in

A

CXCL8

Chemokines

Chemotaxis

58
Q

What are the 5 soluble components of the innate system

A

Cytokines

Histamine

Acute phase proteins

Arachidonic acid metabolites

Soluble inter-related plasma protein systems

59
Q

What is histamine generated from

Where is it stored

A

Histidine

In granules in mast cells, basophils and eosinophils

60
Q

What does histamine do

A

Acts on local blood vessels causing immediate capillary vasodilation

61
Q

What does IL-6 do

A

Stimulates hepatocytes to release acute phase proteins

62
Q

What do acute phase proteins include

A

C-reactive protein (opsonin and complement activation) and fibrinogen

63
Q

What is fibrinogen converted to

How does that help with immunity

A

Insoluble fibrin strands

This can entrap bacteria limiting growth and dissemination and support the recruitment and activation of host cells, facilitating elimination of infecting microbes

64
Q

What are prostaglandins and leukotrienes examples of

A

Potent inflammatory mediators generated after tissue damage

65
Q

What are arachidonic acid metabolites derived from

A

Cell membrane phospholipid’s

66
Q

Where are many of the components of the soluble inter-related plasma protein systems formed

How are these systems activated

A

Liver

67
Q

Name 4 of the soluble interrelated plasma protein systems

A

Clotting system

Kinin system

Fibrinolytics system

Complement system

68
Q

What does the clotting system involve

A

Thrombin which converts fibrinogens into fibrin and fibrinopeptides which form clots to limit the spread of infection

69
Q

Other than fibrinogen, what does thrombin cleave

A

Both C3 and C5

70
Q

What does tissue damage resulting in the kinin system

Which complement components does this system interact with

A

Generation of bradykinin which increases vascular permeability, vasodilation, pain, smooth muscle contraction

Activates C3 and C5

71
Q

What does tissue damage resulting in the fibrinolytic system

Which complement components does this system interact with

A

Generation of plasmin, which degrades fibrin into products that recruit neutrophils

Plasmin activates complement C3

72
Q

Name 3 results of the complement system

A

Opsonisation
Membrane attack complex formation
Generation of anaphylatoxins (C3a, C4a, and C5a)

73
Q

What do fibrinopeptides induce

A

Vascular permeability

Neutrophil chemotaxis

74
Q

Define the acute inflammatory response

A

a stereotypical response to tissue damage or infection

75
Q

How long does the immediate immune response to infection last

What are the 4 key parts of this stage

A

Immediate innate response: 0 - 4hr

complement
Phagocytes
Natural antibodies
Antimicrobial peptides

76
Q

Describe the complement response to the primary infection (4)

A

activation of the alternative (and lectin) pathway rapidly opsonises microbes for phagocytosis.

If natural or specific antibody is present the classical pathway can be used.

Formation of the membrane attack complex (MAC) can destroy pathogens directly.

Complement activation rapidly activates the acute inflammatory response.

77
Q

Describe the phagocytes’ role in the immediate innate response (4)

A

Tissues and mucous membranes contain large numbers of resident macrophages.

These are immediately available to phagocytose pathogens.

They recognise pathogens via an array of complement, scavenger and other
receptors that induce activation and phagocytosis.

Ultimately phagocytes will kill most bacteria.

78
Q

What is the main natural Ab implicated in the immediate innate response to infection

What is it produced by

Is it selected?

A

IgM (reactive against pathogens without prior antigen exposure)

B-1 cells

Possibly selected by self-antigen but is reactive against antigens present on a range of viral, bacterial, fungal and parasitic pathogens

79
Q

What are defensins

What do they do

A

A major group of antimicrobial peptides in humans

disrupt membranes and are effective against Gram-positive and negative bacteria, fungi, parasites and enveloped viruses

80
Q

What produces defensins (5)

A

epithelial cells in skin, respiratory and urogenital tracts (β-defensins) and by Paneth cells
in the small intestine (α-defensins)
neutrophils

81
Q

What happens if an infection is not cleared after 4 hours by the immediate innate response

A

the induced innate immune response begins - this lasts for up to 4 days

82
Q

What are macrophages essential for in the induced innate response to infection

A

recruitment of additional effector cells/molecules;

They possess an array of PRRs that once activated signal production of the proinflammatory cytokines IL-1, IL-6, IL-12 and TNF-α and the chemokine CXCL8.

83
Q

Give 6 things that TNF-α does in the induced innate response to infection

A

induces adhesion molecule expression on vascular endothelium (neutrophil recruitment)

  • increases vascular permeability (inflammatory exudate)
  • triggers platelet activation and blood clotting
  • stimulates dendritic cell maturation and migration to lymph nodes
  • stimulates the acute phase response (in combination with IL-1 and IL-6)
  • primes newly recruited neutrophils
84
Q

When are neutrophils recruited to the site of infection in the induced innate response

What is their role

A

within 6-12 hours

phagocytosis
activation also releases ROS and catabolic enzymes

85
Q

What do the ROS and catabolic enzymes released from neutrophils in the induced innate response to infection do

A

inactivate micro-organisms but can also damage normal tissue (bystander effect)

86
Q

Are monocytes recruited before or after neutrophils in the induced innate response to infection

What do they do when they reach the site of infection

A

recruited later

mature into macrophages which will phagocytose microbes and cellular debris (janitorial role)

87
Q

What are RLRs

What do they do

A

RIG-I-like
receptors

detect the presence of viral nucleic acid in the cytoplasm of infected cells and induce expression of type 1 interferons (IFN-α and IFN-β).

88
Q

What do interferons do after being released from RLRs in the induced innate response to a viral infection (3)

A

induce an antiviral state in surrounding cells by interfering with virus replication (e.g. PKR, OAS and Mx).

Interferons also work indirectly by activating NK cells

IFN-γ plays a major
role in macrophage activation.

89
Q

Where are NK cells present in the body

A

present in most tissues and abundant in blood (5-25% of lymphocytes).

90
Q

What do NK cells do in the induced innate response to infection

A

kill infected host cells and secrete cytokines that act mainly on macrophages to upregulate phagocytosis and inflammatory cytokine expression

91
Q

What activates NK cells at the site of infection

What does this do

Which cells do NK cells interact with after activation (2)

A

IL-12

induce proliferation

macrophages (work in partnership and activate each other)

DCs (may signal the need for initiation of an adaptive immune response)

92
Q

Where are ILCs present

A

in barrier tissues where they respond rapidly to pathogens to eliminate or hinder their spread.

93
Q

How do ILCs and T cells interact

What is the aim

A

The major sunsets of ILCs and CD4 T cells (ILC1/TH1, ILC2/TH2 and ILC3/TH17) work cooperatively.

coordinate adaptive responses with different arms of the myelomonocytic pathway to generate responses appropriate for the particular pathogen

94
Q

Which cells are activated by which t cells

A

monocyte and macrophage being enhanced by TH1 cells;

eosinophils, basophils and mast cells by TH2 cells;

neutrophils by TH17 cells

95
Q

Why does the adaptive response to infection take 4 days to kick in (4)

A

because it requires:
dendritic cell activation and migration to secondary lymphoid organs
• activation of low frequency T cells
• activation and proliferation of antigen-specific B cells by activated T cells
• B cell differentiation into plasma cells for antibody production, B cell isotype switching and affinity maturation

96
Q

How do the 4 different types of T cell act in an infection during the adaptive response

A
  • CTLs are MHC class I restricted and kill cells harbouring intracellular viruses, bacteria and parasites
  • TH1 cells (IFN-γ) are MHC class II restricted and their main role is to activate macrophages
  • TH2 cells (IL-4) direct IgE production and help eosinophils, basophils, mast cells and B cells respond to parasite infections.
  • TH17 cells (IL-17) help neutrophils respond to extracellular fungal and bacterial infections.
97
Q

How long after infection do specific antibodies appear

A

5 days after (this varies and can be longer)

98
Q

What is the first Ig isotype to be produced in the immune response to infection

what does it do (2)

A

IgM

recruits complement very efficiently and can compensate for low affinity through high avidity

99
Q

What is a common theme for all of the 3 types of response to infection

A

innate sentinel cells such as macrophages, dendritic cells, tissue-resident mast cells or epithelial cells sense the presence of pathogens using arrays of pattern recognition receptors and respond by producing cytokines and chemokines

100
Q

what does the production of chemokines and cytokines from innate sentinel cells do during infection

What is the purpose of this early response

A

initiates local inflammation and activates
innate lymphoid cells (ILCs)

helps to contain the infection until an appropriate adaptive response involving dendritic cells, effector T cells and class switched antibody can be made

101
Q

Do ILCs require priming

A

no - they act immediately to enhance the function of resident and recruited innate effector cells

102
Q

What does the type 1 response to infection focus on

Which immune cells does it use (5)

A

n intracellular pathogens such as intracellular bacteria, viruses and parasites.

involve the group 1 ILC1 cells, TH1 cells, NK cells, CTLs, and M1 macrophages

103
Q

What does the type 2 immune response to infection focus on

Which immune cells does this response involve (6)

A

large multicellular parasites e.g. helminths

group 2 ILC2 cells, 
TH2 cells, 
IgE, 
basophils, 
tissue-mast cells, 
eosinophils (which express FcεRI and can be prebound by IgE) 
M2 macrophages
104
Q

What does type 3 response to infection focus on

Which cells are involved (4)

A

extracellular bacteria and fungi

group 3 ILC3 cells, TH17 cells, opsonising antibody isotypes and neutrophils.

105
Q

What happens after macrophages and DCs recognise intracellular pathogens

A

produce IL-12, which stimulates ILC1 and NK cells to produce IFN-γ which induces
macrophages to upregulate their killing capacity

DC cells travel to regional lymph nodes to activate CD4 and CD8 T cells

106
Q

What is the purpose of the production of IFN-γ from ILC-1 and NK cells in response to intracellular pathogens in a type 1 response to infection

A

upregulates macrophage killing capacity

polarises towards Th1 response

107
Q

In the type 1 response to viral infection, how are CTLs activated

How are macrophages induced to increase killing capacity

A

Some viral infections may directly activate CTLs without additional T cell help but many require help from TH1 cells.

by IFN-γ (classical or M1 macrophage
activation)

108
Q

How do NK cells and CTLs kill infected cells in the type 1 response to infection

A

directly kill infected cells by release of perforin and granzyme.

109
Q

How are chronically infected bacteria laden macrophages dealt with in the type 1 response to infection

A

perforin from NK cells and CTLs

or by Th1 cells via Fas/Fas dependent apoptosis , which releases the bacteria to be killed by fresh macrophages

110
Q

Describe the steps involved in controlling a viral infection using the Type 1 response

A
  • Interferon initiates an antiviral state
  • NK cells a) kill virally infected cells and b) secrete inflammatory cytokines, which act on macrophages to enhance phagocytosis of viral particles and induce macrophage cytokine secretion
  • NK killing is enhanced 20-100 fold by IFN-β, IFN-α or IL-12. This contains infection until adaptive immunity is generated.

• CTLs kill virally infected cells
The adaptive cell-mediated response to virus relies mainly on cytotoxic CTL and helper TH1 cells.

111
Q

What is the time scale for CTL activity against viral infections in a type 1 response to infection

A

For many virus infections CTL activity arises around days 3-4, peaks at days 7-10 and then declines.

112
Q

How does protective immunity generated through infection or vaccination mainly work

A

through neutralising antibodies

113
Q

What are the steps involved in killing intracellular bacteria

A
  • Neutrophils and macrophages phagocytose pathogen
  • Macrophage ->IL-12 -> activates NK cell/TH1 cell -> IFN-γ -> activates macrophages to upregulate killing.
  • Adaptive response: CD8-CTLs directly kill infected cells. CD4-TH1 cells express CD40L and activate macrophages more strongly than IFN-γ alone. TH1 cells can induce Fas/Fas ligand-dependent apoptosis of chronically infected cells.
  • Generation of a memory T cell response is required to protect against most intracellular bacteria.
114
Q

What is the main innate response to protozoa

What is a problem with this strategy? Give an example

A

phagocytosis

resistance to phagocytic killing is
common (e.g. T. gondii limits parasitophorous vacuole acidification and lysosome fusion).

115
Q

How to epithelial cells respond to helminths early in infection

A

secreting alarmins, which activate ILC2 cells present in mucosal sites

116
Q

Name 3 alarmins

When are they produced

What do they do

A

thymic stromal lymphopoietin (TSLP), IL-25 and IL-33

produced by epithelial cells in an early response to helminth infection

ILC2 cells present in mucosal sites are activated by these alarmins and produce IL-13 and IL-5.

117
Q

What do the following do in helminth infection
IL-13

IL5

A

IL13: stimulates smooth muscle contraction, increased
epithelial cell turnover and mucus production by goblet cells.

IL5: stimulates eosinophil recruitment and activation

118
Q

Which Th response is favoured in the presence of IL13 and TSLP

What else helps drives this

A

Th2

IL-4 (from an unknown source, maybe basophils, mast cells or iNKT cells)

119
Q

At the site of helminth infection, what do Th2 cells do?

A

enhance the recruitment and function of type 2 innate effector cells, eosinophils, basophils, tissue-mast cells and alternatively activated M2 macrophages.

also drive IgE production

120
Q

What do eosinophils do in helminth infection

A

When directed by surface bound IgE, eosinophils release cytotoxic molecules stored in secretory granules directly onto the worm surface (e.g. major basic protein, MBP).

121
Q

What do mast cells do in the type 2 response to helminth infection

What does this lead to

A

Mast cells armed with helminth specific IgE produce mediators including histamine, TNF-α, prostaglandins & leukotrienes and proteases such as mucosal mast cell protease-1

increased vascular and epithelial permeability, mucus production, intestinal motility and leucocyte recruitment creates a ‘weep and sweep’ environment that helps expel parasites

122
Q

What do macrophages do in the type 2 response to infection

A

M2 macrophages increase smooth muscle contraction and control tissue repair and remodelling.

These TH2-activated macrophages are also important in forming granulomas that entrap worm larvae in tissues

123
Q

What is the type 3 response to infection important for

A

at barrier sites to control extracellular bacteria and fungi (including components of microbiota that enter when the barrier epithelium is damaged)

124
Q

What is the sequence of actions that occurs during the type 3 response to infection

A

ILC3 cells respond rapidly to IL-23 produced by mononuclear phagocytes after recognition of bacterial/fungal PAMPs.

They produce IL-17 and IL-22.

The action of these cytokines may indirectly promote the generation of the subsequent TH17 response by increasing local levels of IL-1β, IL-6 and IL-23.

125
Q

What does IL-17 do in the type 3 response to extracellular infection

A

stimulates local stromal cells, epithelial cells and myeloid cells to produce proinflammatory cytokines and chemokines (e.g. IL-1β, IL-6, GM-CSF and CXCL8), which recruit neutrophils

126
Q

What does IL-22 do in the type 3 response to infection

A

increases epithelial cell division and shedding to impair bacterial colonisation.
Works with IL-17 to produce antimicrobial peptides (AMP) and promote barrier integrity

127
Q

How do ILC3 and Th17 work together in the type 3 response to infection

A

Whilst ILC3 cells respond rapidly TH17 cells amplify and sustain the production of IL-22 giving long lasting protection at sites of infection

128
Q

What do Tfh cells do in a type 3 response to infection

Is this effective

A

promote high affinity IgG and IgA responses and plasma cells secreting these localise to barrier tissues.

yes- Antibodies clear
many primary infections with bacteria such as Staphylococcus aureus and Streptococcus pneumoniae which elicit type 3 responses

BoD (11 decks)

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