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Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What is the immune system?

A

A collection of cells and chemicals that work together to protect us from disease

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2
Q

Where are leukocytes produced?

A

Red Bone Marrow

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3
Q

What types of immunity does Innate immunity involve

A

Humoral and cellular immunity

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4
Q

What does innate humoral immunity involve?

A

Proteins dissolved in serum, plasma and tissue fluid

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5
Q

What proteins does innate humoral immunity involve?

A

Acute phase, complement proteins and antibodies

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6
Q

What is cellular immunity?

A

Cells which have mechanisms to identify and kill foreign organisms
Cellular immunity occurs inside infected cells and is mediated by T lymphocytes. The pathogen’s antigens are expressed on the cell surface or on an antigen-presenting cell
slower

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7
Q

What has to happen for innate immune response to start?

A

Pathogens must breach physical barriers

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8
Q

What immune cells are involved in innate response?

A

Phagocytes (neutrophils and macrophages) and natural killer cells

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9
Q

What ways can a pathogen enter the body?

A

Respiratory tract, skin, eyes, gastrointestinal tract, genitourinary tract

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10
Q

What physical barriers does the body have to prevent pathogen entry?

A

Wax, hair, tears (lysozymes), mucus, membranes, specialist epithelial cells, air movement

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11
Q

What physical barriers are there to pathogens outside of the body

A
  1. Air flow
  2. Antimicrobial Enzymes e.g lysozymes in tears
  3. Low pH (skin has sebum that contains fatty acids)
  4. Defensins- antimicrobial peptides that destroy the cell membrane
  5. Normal microbiota/flora of skin outcompete pathogens- reduce space nutrients for pathogen entering
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12
Q

What physical barriers are there once pathogen has entered body tissue?

A
  1. Epithelial cells tight junctions- restrict microorganisms moving deep into tissue
  2. Goblet cells- secrete mucus that is sticky and traps bacteria
  3. Ciliated cells - cilia waft to push and flush out pathogens
  4. Immune cells in the tissue- phagocytes phagocytose pathogens
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13
Q

What happens if the barriers are breached?

A

Cells are damaged and exposed to the environment

A bump/cut can initiate inflammatory response even without presence of pathogen

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14
Q

What is inflammation?

A

Body’s response to damage to protect itself
Located to the site of damage and involves the immune response
Has a series of stages and is resolved and tissue returns to normal

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15
Q

Stages of inflammation?

A
  1. innate immune cells e.g basophils, eosinophils and platelets release histamine and cytokines
  2. Histamine binds to histamine receptors
  3. Histamine causes vasodilation of blood vessels resulting in localised heat and redness
  4. Increased temperature prevents pathogen colonising and reproducing
  5. Histamine causes blood vessels to become more leaky= exudation of fluid from blood into tissue
  6. Causes swelling (odema) and pain
  7. Cytokines attract phagocytes to infection site
  8. Phagocytes kill pathogen by phagocytosis
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16
Q

Signs of Inflammation

A 
Rubor= Redness
Calor= Heat
Tumor= Swelling
Dolor= Pain
Functio Laesa= Loss of function
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17
Q

Receptor-Ligand Interactions

A
  1. Receptor binds to ligand
  2. Causes a conformational change in receptor
  3. Causing signal to change gene expression
    Immune system works by turning ligand-receptor interactions on/off
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18
Q

What happens when no microbes are present?

A
  1. Damaged cells are released into fragments
  2. Fragments contain Damage Associated Molecular Patterns (DAMPs)
  3. DAMPs bind to receptors
  4. Cytokines released
  5. Inflammation Triggered
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19
Q

Examples of DAMPs

A

DNA, RNA, proteins in nucleus

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20
Q

What happens when microbes enter the wound?

A
  1. Microbes enter body
  2. Microbes release chemicals that body sees as ‘foreign’
  3. Some microbes are pathogenic and can grow within the tissue causing more damage to cells.
  4. Some pathogenic microbes can enter cells living inside of them.
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21
Q

What immune response deals with Extracellular pathogens?

A

Humoral Immunity

By soluble factors: Antibodies, acute phase proteins, (e.g C reactive protein) and complement

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22
Q

What immune response deals with intracellular pathogens?

A

Cell mediated immunity

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23
Q

What are Acute Phase Proteins?

A

Proteins that change their serum concentration by >25% in response to inflammatory cytokines
They can have pro/anti or both inflammatory effects

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24
Q

Where are acute phase proteins released from?

A

Liver

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25
Q

What do Acute Phase Proteins bind to?

A

Bind to pathogens and destroy them

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26
Q

3 examples of Acute Phase Proteins released from the liver

A
  1. C-reactive protein
  2. Fibrinogen
  3. Mannose-binding lectin
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27
Q

What does C-reactive protein do?

A
  1. promotes binding of complement= enhancing phagocytosis by macrophages
    It is an acute marker of inflammation
    Levels increase dramatically during inflammation
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28
Q

What is the complement system?

A

Made up of a large number of distinct plasma proteins (C1-C9) that react with one another to opsonize pathogens and induce a series of inflammatory responses that help to fight infection
Activated when C1q binds to antibody attached to antigen (IgG bound to antigen)

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29
Q

3 outcomes of the complement pathway?

A
  1. Opsonisation/Phagocytosis
  2. Chemotaxis
  3. Membrane Attack Complex
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30
Q

What is chemotaxis?

A

C3a and C5a recruit phagocytes to infection site and promote inflammation
C3A and C5a can increase permeability of blood vessels and activate mast cells

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31
Q

What are some chemotactic factors?

A
  1. Products of injured tissue
  2. Factors from blood e.g C5a
  3. Histamine released from mast cells and neutrophils
  4. Bacterial products
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32
Q

What factor forms membrane attack complex?

A

C3b combines with C3 convertase= C5 convertase
C5 cleaved into C5a and C5b
C5b recruits C6,C7 then recruits C8
Causes polymerisation of C9 in membrane
Poly C9 protein in cell membrane = C5b6,7,8-9= Membrane attack complex

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33
Q

3 pathways of the complement system

A

Classical Pathway
Lectin Pathway
Alternative Pathway

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34
Q

Which of the pathways are antibody dependent?

A

Classical pathway

Needs an antibody/antigen complex to trigger it

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35
Q

What antibodies are involved in the complement pathway?

A

IgM and IgG

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36
Q

How is the membrane attack complex formed?

A

When complement enzymes cleave C5

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37
Q

What are C1-C9 proteins cleaved into?

A

a and b fragments

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38
Q

a fragment

A

smaller, inactive

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39
Q

b fragment

A

larger, active

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40
Q

What does C3a help in?

A

Inflamamtion

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41
Q

Membrane attack complex

A

Influx of Ca2+ into cell

causing osmotic lysis

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42
Q

Which 2 pathways are antibody-independent?

A

Lectin Pathway and Alternative Pathway

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43
Q

What initiates the lectin pathway?

A

Pathogen membrane containing Mannose

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44
Q

Components pf the alternative pathway

A

Factor B, Factor D, properdin protein

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45
Q

Innate Lymphoid Cell

A

Don’t express antigen-specific receptors

Release cytokines

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46
Q

How do innate immune cells find and detect pathogens?

A
  1. Damaged cells release DAMPs
  2. DAMPs bind to receptors on immune cells (mainly macrophages and dendritic cells)
  3. this activates transcription pathways to kill pathogen
  4. PAMPs also bind to immune cells to make them aware of infection
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47
Q

What do DAMPs and PAMPs bind to?

A

Pattern Recognition Receptors

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48
Q

Where are PRRs found?

A

Surface of macrophages and dendritic cells

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49
Q

Examples of common PAMPs

A
  1. Spike Coat Proteins on DNA/RNA viruses
  2. LPS
  3. LTA
  4. Flagellin
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50
Q

Where is LPS found?

A

Outer membrane of Gram negative bacteria

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51
Q

Where is LTA found?

A

Cell wall of gram positive bacteria

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52
Q

Types of Pattern Recognition Receptors

A
  1. External PRRs
  2. internal PRRs
  3. Phagocytic Receptors
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53
Q

Name of external PRRs

A

Toll like receptors

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54
Q

Name of Internal PRRs

A

NOD-RIG like receptors and endosomal receptors

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55
Q

Where are internal PRRs found?

A

Cytoplasm of immune cells

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56
Q

How may toll like receptors are there

A

9

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57
Q

Homodimer TLRs

A

TLR 4

TLR 5

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58
Q

Heterodimer TLR

A

TLR 2 binds to TLR 1/6

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59
Q

Which TLRS are external?

A

TLRS 1,2,4,5,6

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60
Q

Which TLRs are inside immune cell?

A

TLRs 3,7,8,9 (all homodimer)

61
Q

What does TLR 3 bind to?

A

Double stranded RNA

62
Q

What does TLR 7 bind to?

A

Single Stranded RNA

63
Q

What does TLR 8 bind to?

A

Single Stranded RNA

64
Q

What does TLR 9 bind to?

A

CpG DNA

65
Q

What cells is TLR 2&1/6 found on?

A 
Monocytes 
Dendritic cells 
Mast cells
Eosinophils
Basophils
66
Q

What cells is TLR 5 found on?

A

Intestinal epithelium cells

67
Q

What cells is TLR 4 found on?

A

Macrophages
Dendritic cells
Eosinophils
Mast cells

68
Q

What are cytokines?

A

Chemical mediators of cell to cell communication

69
Q

What are pro-inflammatory cytokines?

A

Signal cells there is danger

Activate immune cells and induce inflammation

70
Q

Examples of pro-inflammatory cytokines

A

Tumour necrosis factor (TNFα)
IL-6
IL-1 beta

71
Q

What are anti-inflammatory cytokines?

A

Signal cells that there is no danger

Turn off inflammation

72
Q

Examples of anti-inflammatory cytokines

A

IL-10

Transforming Growth Factor beta (TGFβ)

73
Q

IL-6

A

Earliest cytokine released by damaged cell

Causes release of acute phase proteins from liver

74
Q

What releases cytokines?

A

Macrophages

75
Q

What do cytokines do?

A
  1. Cytokines released by macrophages signal hypothalamus to increase temperature= fever
  2. Signal bone marrow to increase WBC production
  3. Cause blood vessel walls to become leakier
76
Q

Process with PRRs

A

PAMPs/DAMPs bind to PRRs
Causes immune cells to release cytokines/chemokines
Chemokines attract WBC to site of infection
Pathogen binds to PRR
Pathogen is engulfed and phagocytosed by macrophage/neutrophil

77
Q

How do macrophages kill the pathogen?

A
  1. pathogen is recognised by PRR
  2. Macrophages are activated
  3. Phagocytosis is induced
  4. The pathogen is internalised in a phagosome by pseudopodia- The actin filaments in the cytoplasm push the cell membrane
  5. Phagosome fuses with a lysosome containing antimicrobial peptides, enzymes and reactive oxygen species= phagolysosome
  6. Activated macrophages make pro-inflammatory cytokines which attract and activate other immune cells
  7. The pathogen is killed by oxidative burst and digested by enzymes
78
Q

How do the immune cells find the pathogen?

A

Chemokines are made by macrophages

Immune cells will move to the area of the highest chemokine concentration

79
Q

What do neutrophils do when they arrive?

A
  1. Phagocytosis
  2. Netosis
  3. Killed by apoptosis when they are exhausted as they are v short lived
80
Q

What is netosis?

A

Neutrophils create extracellular nets= meshwork of DNA, sugar and proteins that trap microbes

81
Q

What happens if pathogen isn’t cleared?

A

Pro-inflammatory cytokines are still released
Causing systemic infection/inflammation
Damaged blood vessels release bradykinins- continues to increase vascular permeability
Results in chronic inflammation

82
Q

What do bradykinins do?

A

Increase vascular permeability of damaged blood vessels
Stimulates nerves
Causing pain

83
Q

What diseases can chronic inflammation lead to?

A

Rheumatoid arthritis

Multiple sclerosis

84
Q

Example of an intracellular pathogen

A

Mycobacterium Tuberculosis

85
Q

Why cant humoral response get rid of intracellular pathogens?

A

Humoral response wouldn’t be able to access pathogen inside the cell

86
Q

How do cells recognise intracellular pathogens?

A
  1. DAMPs released by damaged cells by the pathogen are recognised by intracellular PRRs
  2. PAMPs released from cell activate innate immune cells
  3. Infected cells can flag themselves to show immune system they are infected
87
Q

Most common intracellular pathogen

A

Viruses

88
Q

How are Natural Killer cells and Adaptive immune cells activated?

A

By cytokines

89
Q

What happens once DAMPs and PAMPs bind to intracellular Endosomal Toll-Like receptor?

A

Interferons are released

90
Q

What do interferons do?

A
  1. Interferes with viral replication
  2. Enhances killing power of NK and cytotoxic cells
  3. Enhances phagocytosis by macrophages
  4. Stimulates production of antibodies
  5. Slows cell division and tumour growth
91
Q

What else do Interferons bind to?

A

Surface of uninfected cells

92
Q

What do interferons cause uninfected cells to do?

A
  1. Prevent viral replication by introducing transcription pathways
  2. Cause uninfected cells to change their surface to prevent pathogen entery
93
Q

Function of interferons

A

Increase viral defences and reduce viral replication in nearby uninfected cells

94
Q

What are the anti-viral mechanisms of interferons?

A

Type 1 interferons= IFNa and β bind to IFNa receptor

These activate genes that degrades viral RNA and halts protein synthesis needed to make viral capsules

95
Q

What do type 1 interferons also activate?

A

Natural killer cells

96
Q

Interferon a and b

A

Feedback loop between these 2

- if IFN-B is produced first
- It binds to receptors
- Causes amplification of IFNa to be made
- (IFNβ increases production of IFNα amplifying the response)
97
Q

What do Natural Killer Cells do?

A

Kill virally infected and cancer cells by apoptosis

98
Q

How do NK cells kill cells?

A
  1. NK cells activate Interferon Gamma (IFNγ) and Interferon a (IFNa)
  2. These interferons activate other immune cells
  3. NK cells release perforin and granzyme
99
Q

What does perforin do?

A

Punctures holes in cell wall

100
Q

What does granzyme do?

A

Degrades pathogen= apoptosis

101
Q

How do NK cells know which cells to kill when none of them are foreign?

A

A normal healthy cell is normally covered in inhibitory ligands
But in cancer and virally infected cells these are degraded
Cancer and virally infected cells up regulate activating ligands
So these cells are coated in activating ligands

102
Q

What does antimicrobial lysozyme do?

A

Digest bacterial cell wall

103
Q

What does antimicrobial peptide defensin do?

A

Lyse bacterial cell wall

104
Q

Does innate immunity provide long term immunological memory?

A

No

105
Q

Once physical barriers are broken what are the 2 stages of innate immunity?

A
  1. Antimicrobial enzymes, peptides, complement system

2. Recognition of PAMPs by immune cells- acute phase proteins, inflammation

106
Q

3 stages of response to initial infection

A
  1. Innate immunity
  2. Induced innate immunity
  3. Adaptive immune response
107
Q

Some anatomic barriers?

A

Phagocytes (macrophages) below epithelia- engulf and digest pathogen
Antimicrobial enzymes/peptides

108
Q

Route of entry of pathogen into body

A

GI tract
Respiratory tract and mouth
Urogenital tract
external surface- wounds and abrasions/insect bites

109
Q

Pathogenesis meaning

A

Means by which pathogen causes disease and host response

110
Q

Why can’t staphylococcus and streptococcus bacteria be killed by phagocytes?

A

They have protective polysaccharide capsule that prevents phagocyte entering for phagocytosis
This activates the complement pathway

111
Q

Mycobacteria characteristics

A

Facultative intracellular pathogens
Can replicate inside/outside of cell
Arabinogalactan

112
Q

Why wouldn’t innate immunity be helpful in removing toxins?

A

Highly specific antibody is needed to neutralise toxins

So adaptive immunity is required

113
Q

Example of an endotoxin

A

LPS in outer membrane of gram negative bacteria

114
Q

What do endotoxins trigger phagocytes to do?

A

Release cytokines

115
Q

How does adaptive immunity differ from innate immunity?

A

AA targets structures specific to a particular strain or variants of a pathogen
AA provides immunological memory

116
Q

How does extracellular bacteria cause disease?

A

Release exotoxins

117
Q

What do mucosal epithelium secrete?

A

Mucus (mucins=glycoproteins)

118
Q

How does mucus help?

A

Mucus coats MO
Prevents MO adhering to epithelium in respiratory tract
MO flushed out by beating cilia once trapped by mucus

119
Q

Why is peristalsis important?

A

keeps food and infectious agents moving through the body

if no peristalsis= accumulation of pathogenic bacteria in gut lumen

120
Q

What is microbiota/commensal bacteria?

A

Non-pathogenic bacteria in the body

121
Q

What does commensal bacteria do?

A

Competes with pathogenic MO for nutrients and attachment to epithelia surfaces

122
Q

How does commensal bacteria compete with pathogenic MO?

A

Produce antimicrobial peptides (bacteriocins)
Produce antimicrobial substances e.g lactic acid
Strengthen barrier functions of epithelia which stimulates epithelia cells to make AM peptides

123
Q

How does lysozyme kill bacteria cell wall?

A

Breaks chemical bond in peptidoglycan
More effective in gram positive than gram negative bacteria as cell wall in gram positive is exposed
in gram negative= cell wall covered by outer membrane LPS

124
Q

How do defensins cause lysis of bacteria cell wall?

A

Insert ots hydrophobic region into membrane bilayer
Create pores in cell wall= leaky
= lysis

125
Q

What does C5a in do complement system?

A

Stimulates respiratory burst in phagocytes
Acts as chemoattractant for neutrophils and monocytes
Promotes inflammation by increasing vascular permeability (bradykinin)
Activates mast cells- release granules containing histamine and TNF-alpha= pro inflammation

126
Q

What happens in induced innate response?

A

PPRs (TLRs) stimulate macrophages and dendritic cells by PAMPs

127
Q

What do macrophages and dendritic cells secrete in induced innate immunity?

A

Cytokines and chemokines

128
Q

What are chemokines?

A

Family of chemoattractant proteins

role in leukocyte migration

129
Q

What do chemokines released by macrophages and dendritic cells do?

A

chemoattractants for leukocytes

recruits monocytes and neutrophils and otjer effector cells from blood to site of infection

130
Q

What is the first immune cell to arrive at a site of infection?

A

Neutrophils

131
Q

Which cells are recruited to site of infection after neutrophils?

A

Monocytes, immature dendritic cells

132
Q

What do cell adhesion molecules do during an inflammatory response?

A

Control interactions between leukocytes and endothelial cells on blood vessels

133
Q

During inflammation what cells cross the blood vessel wall and enter inflamed tissue?

A

Neutrophil

134
Q

What do cytokines released by macrophages and dendritic cells activate?

A

acute phase proteins

135
Q

What do acute phase proteins do?

A

Bind to pathogen
Act as opsonins
Activates classical pathway in complement system

136
Q

Examples of acute phase proteins

A

C-reactive proteins
serum amyloid proteins
fibrinogen

137
Q

What do pro-inflammatory cytokines(released by macrophages) cause?

A

Local effect- inflammation and repair

Systemic effect- fever, leukocytosis (accumulation of WBCs)

138
Q

Local effects of pro-inflammatory cytokines?

A

Inflammation

Repair- activate fibroblasts to cause cell proliferation and collagen synthesis

139
Q

Systemic effects of pro-inflammatory cytokines?

A

Fever (signal hypothalamus to increase body temp= prevent pathogen colonising)
Leukocytosis- recruit neutrophils and monocytes to inflammation site (monocytes become macrophages when enter tissue)
Neutrophil PRRs bind to PAMPs= phagocytosis

140
Q

What happens during inflammation?

A

PAMPs of pathogen activate immune cells- macrophages and mast cells
Mast cells release histamine (from their granules)
Macrophages release pro-inflammatory cytokines

141
Q

What are C3a and C5a?

A

Promote inflammation
They are chemoattractants- attract immune cells
Increase vascular permeability

142
Q

What do dendritic cells/macrophages do once they have become activated APCs during inflammation?

A

Travel to lymph node (by chemokines)
Dendritic/macrophage APC attracts naive B/T cells
B cell= plasma cells= antibody
T cell= T helper/cytotoxic

143
Q

Chemotactic factors

A 
C3a 
C5a
Recruit neutrophils
Increase vascular permeability
Induce mast cells
144
Q

In the complement cascade what acts as opsonins?

A

C4b, C1q, C3b

145
Q

How is the complement cascade activated?

A

C1q binding to antibody(Ig M/IgG) (antibody-antigen complex)

146
Q

What is the main component of membrane attack complex in complement cascade?

A

C9

147
Q

What cytokine is produced once bacteria is cleared and tissue is clearing

A

IL-10 (anti-inflammatory)

148
Q

What interferons activate NK cells?

A

Type1- alpha and beta

Immunology (7 decks)

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