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Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What is the immune system?

A

Collection of cells and chemicals which work together to protect us from disease

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2
Q

Where are immune cells (leukocytes) produced?

A

Bone marrow

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3
Q

What produces immune chemicals?

A

Immune cells (but also all body cells - alert immune cells to infection in rest of body cells - switch on)

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4
Q

Immune chemical example?

A

Cytokines

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5
Q

Where are immune cells?

A

-Blood
-Body tissues
-Immune organs

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6
Q

What does body need protecting from?

A

-Toxins (cancer)
-Pollution (cancer)
-Fungi
-Viruses
-Parasites
-Bacteria

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7
Q

What are characteristics of the innate immune system?

A

-Non-specific
-Fast

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8
Q

What are the characteristics of the adaptive immune system?

A

-Specific to a pathogen - finds specific cells to target specific pathogen
-Slower

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9
Q

Interaction between innate & adaptive immune systems?

A

Innate initiates adaptive & then adaptive will ‘help’ innate function better - shown by overlap in humours & cellular immunity

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10
Q

What is humoral immunity?

A

Proteins dissolved in serum, plasma & tissue fluid
Soluble/liquid parts of immune system
-Innate = compliment proteins
-Adaptive = antibodies

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11
Q

What is cellular immunity?

A

Cells with mechanisms to identify & kill foreign organisms
Insoluble
Cell actively work on pathogens

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12
Q

What are the stages of the immune response?

A
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13
Q

What components are involved in innate immunity?

A

-Epithelial barriers
-Compliment proteins
-Phagocytes
-Natural killer cells
-Dendritic cells

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14
Q

What components are involved in adaptive immunity?

A

-Dendritic cells
-B cells
-T cells
-Antibodies
-Effector T cells
-Memory T & B cells

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15
Q

How fast does innate immune system start?

A

In minutes - rapidly

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16
Q

How fast does adaptive immune system start?

A

Faster if already have immunity - i.e., memory cells
1st time = a week
Memory = 1-7 days

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17
Q

Where can microbes enter body?

A

-Skin
-Resp tract
-Eyes
-GI tract
-Genitourinary tract
—> so have physical defences

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18
Q

Examples of physical barriers?

A

-Hair
-Wax
-Membs (hard to penetrate)
-Spec do cells (e.g., ciliated ep cells)
-Tears (enzymes e.g., lysozymes)
-Mucus (toxic, sticky, contains anti-microbials)
-Air movements

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19
Q

What are the barrier defence found at physical defences?

A

-Air/fluid flow
-Enzymes
-Low pH
-Defensins
-Normal microbiota
-Ep cell tight junctions
-Goblet cells
-Ciliated cells
-Tissue resistant immune cells

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20
Q

How does air/fluid act as a barrier defence?

A

Prevents microorganisms attaching

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21
Q

How do enzymes acts as barrier defences?

A

Secretions contains antimicrobials

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22
Q

How does low pH act as a barrier defence?

A

Affects protein structure (denatures some) - so few pathogens survive if ingest

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23
Q

How do defensins act as a barrier defence?

A

= antimicrobial peptides - affects cell memb & viral envelopes

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24
Q

How does normal microbiota act as a barrier defence?

A

Outcompetes potentially harmful organisms
-Live symbiotically w/ us
-In upper mucus layer - don’t contact our cells

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25
Q

How do ep cell tight junctions act as a barrier defence?

A

Prevents microorganisms moving deeper into tissues
EP cells = tightly together

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26
Q

How do goblet cells act as a barrier defence?

A

Make mucus = sticky barrier - pulls microbes away from cells

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27
Q

How do ciliated ep cells act as a barrier defence?

A

Push mucus along - moves pathogens out

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28
Q

How do tissue resident immune cells act as a barrier defence?

A

-Recognise
-Phagocytose (engulf)
-Kill pathogens
-If die can replace by progenitors in blood

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29
Q

What part of immune response is inflammation a part of?

A

Innate

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30
Q

Do pathogens need to be present to trigger inflammation?

A

-NO
-Bump/cut = ep cell damage releases chemicals (DAMPs) - signal to body - physical barriers have been broken

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31
Q

What is inflammation?

A

Response to damage to protect
* Often localised to the site of damage
* Series of stages until = resolved - tissue
returns to normal

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32
Q

What are the hallmarks of acute inflammation?

A

-Redness = Rubor
-Heat = Calor
-Swelling = Tumor
-Pain = Dolor
-Loss of function = Functio laesa

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33
Q

How can acute inflammation progress to chronic/systemic?

A

Chemicals released locally move systemically

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34
Q

What are ligands often in the immune system & what are they called?

A

Cytokines = e.g., interleukin (IL)

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35
Q

What are recs often in the immune system?

A

Cluster of differentiation -> CD

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36
Q

How are signals passed to recs (rec:lig interactions)?

A

-Integration & amplification by cytoplasm
-Target = altering gene expression in nucleus

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37
Q

Process of inflammation?

A

-Ep cell damage = chemokines released
-Ep cells damaged, local mast cells & basophils = release histamine
-Histamine binds to histamine recs on endo cells of blood vs (caps)
-Causes vasodilation (inc permeability) - as ep cells move apart - neutrophils (attracted to injury site - chemicals)
-Neutrophils marginalise, roll, adhere, migrate (along chemokine gradient) - enter tissues
-Exudation = fluid moves from blood -> tissues too
-Neutrophils phagocytose pathogens

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38
Q

What causes swelling in inflammation?

A

Vasodilation

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39
Q

What causes heat in inflammation?

A

Friction of cells again capillary endo wall

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40
Q

What causes redness in inflammation?

A

Red cell accumulation in area

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41
Q

How is inflammation driven long term (until tissue repaired)?

A

Using pro-inflammatory cytokines

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42
Q

What are DAMPS, how do they work?

A

= Damage-Associated Molecular Patterns
-Fragments of OUR cells - not normally released (only when OUR cells are damaged)
-Is DNA, RNA, prots from nuc
-Bind to recs (Pattern recognition recs) = activates - cytokines released
-Inflammation continued

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43
Q

How are microbes recognised as foreign once enter?

A

By PAMPS

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44
Q

What are the 2 types of pathogens?

A

-Live extracellularly - in CT = bacteria, fungi, parasites - normally (viruses = when not entered cell yet or moving to others)
-Live intracellularly = viruses - normally

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45
Q

What immune responses are for each pathogen type?

A

-Ext = humoral
-Int = cell mediated

46
Q

Where is humour found?

A

Serum & plasma

47
Q

What is involved in humoral response?

A

-Acute phase proteins
-Complement proteins
-Antibodies (LATER!)

48
Q

What are acute phase proteins?

A

-Involved in v. early innate response
-Immediately released from liver due to cytokine release from tissues damage/infection

49
Q

What is the complement pathway?

A

-C number enzymes present all time in blood but = inactive
-Infection = 1/3 pathways activated
-Enzymes continually cleave (cut) each other

50
Q

When is complement pathway triggered?

A

As soon as ep barriers breached

51
Q

What is the aim of the memb attack complex?

A

Produce lots of memb attack complex - to fill with water (disrupts cell wall) - cause to lyse (self-destruct)
-Causes blebbing of pathogen

52
Q

What causes memb attack complex?

A

C3b binding to microbe

53
Q

What are the 3 outcomes of comp pathway?

A

-Opsonisation
-Chemotaxis
-Memb attack complex

54
Q

What is opsonisation?

A

Comp prots - C3b - coat pathogen surface - so phagocytes can identify/recognise (using comp recs) & engulf more easily (phagocytosis/pinocytosis)

55
Q

What is chemotaxis?

A

-C3a & C5a recruit phagocytes & cause inflammation
-Causes by molecules cleaved off of enzymes

56
Q

What activates the alternative pathway?

A

Spontaneous
(binding of C3b to microbe)

57
Q

What activates the classical pathway?

A

Antibodies (i.e., if have come across pathogen before)

58
Q

What activates the lectin pathway?

A

Recognise sugars on pathogens (acute phase proteins - liver - MBL)

59
Q

What are DAMPs?

A

= Damage Associated Molecular Patterns
-Released onto our normal cells if damaged
-Bind to recs (Pattern recognition recs) = signals to innate immune cells there is damage

60
Q

What are PAMPs?

A

= Pathogen Associated Molecular Patterns
-Things within pathogens not in OUR cells
-Bins to recs (Pattern recognition recs)
= signals to innate immune cells there is infection (as can be damage but no infection)

61
Q

Examples of PAMPs?

A

-Diff sugars in walls
-Diff prots in capsules
-Diff DNA & RNA orders - C&G repeats
-Flagellum
–> patterns in pathogens

62
Q

What do DAMPs & PAMPs bind to?

A

Pattern Recognition Recs (PRRs)
-Diff cell types have diff PRRs

63
Q

What do PRRs do?

A

Recognise diff types of pathogen

64
Q

What are the types of PRRs?

A

-Phagocytic recs
-Toll like recs (ext & int - in endosomes)
-NOD & RIG - like recs

65
Q

What are phagocytic PRRs?

A

Once activated by PAMPs binding = cause phagocytosis

66
Q

What are ext toll like PRRs?

A

-On cell memb
-Detect infections in ext env

67
Q

What are int/endosomal toll like PRRs?

A

-In memb of endosomes
-Signal to nuc to change role

68
Q

What are NOD & RIG - like PRRs?

A

-Free in cytoplasm (NOT in memb)
-Detects ext pathogens or ones taken up by phagocytes

69
Q

What do toll like (int & end), NOD & RIG - like all cause?

A

Change in gene transcription causing cytokine release

70
Q

How do phagocytic PRRs work?

A

-Pathogen PAMP binds to rec
-Causes phagocytosis - engulf = phagosome
-Enzymes break down pathogen
-Oxidative stress in vesicle = pathogen killed

71
Q

What are some types of phagocytic PPRs x5 & what do they do?

A

-Complement receptor (CR1) = recognises C3b comp protein on pathogen surface

-Scavenger receptors = recognises lipoproteins in bacterial cell walls

-Mannose receptor = recognise mannose on surface of some bacteria

-Fc receptors = recognises antibody bound to pathogen surface

-C-type lectin receptors = recognises β-glucan sugar in fungal cell walls

72
Q

What are the 9 types of toll like PRRs?

A

Plama memb/ext
TLR4 = binds to lipid polysaccharides (LPS) on bacterial cell walls
TLR5 = binds to flagellin = makes motility on bacteria
TLR2 - partnered (dimered) w/ TLR1 or TLR6 = binds to lipoproteins in fungi or bacteria

Endosomal - all bind to viral ‘things’
TLR3 = binds to dsRNA
TLR7 = binds to ssRNA
TLR8 = binds to ssRNA
TLR9 = binds to CpG in DNA

73
Q

How do toll like PRRs work (ext)?

A
  1. PAMP binds to a PRR = signals to nucleus
  2. Adaptors containing TIR signalling domains (e.g., MyD88) transmit message into cytoplasm
  3. Protein TF (called NFκB) assembles & binds to DNA - changes gene expression
  4. = causes cells to produce new proteins
    which initiate the next stage of the immune
    response (inflammatory aspects)
74
Q

What are all of the things called that PRRs bind to?

A

PAMPs & DAMPs

75
Q

What is NFκB?

A

Characteristic inflammatory TF

76
Q

Which toll like PRRs are in which cell types?

A

-TLR 1/2 & TLR 2/6 = monocytes, dendritic cells, eosinophils, basophils & mast cells
-TLR 5 = intestinal ep
-TLR4 = macrophages, dendritic cells, mast cells, eosinophils

77
Q

What happens after immune cells activated (PAMPS)?

A

*Cell communication via:
(damaged cells or macrophages start this to communicate to blood cells –> then blood cells communicate w/ tissue cells)
-Cell-to-cell contact (rec of 1 binds to something on other)
-Cytokine release = diffuse to blood bind to distant recs on immune cells

78
Q

What are cytokines?

A

Responsible for cell-to-cell communication at a distance

79
Q

What are the 2 types of cytokines?

A

1 = proinflammatory –> signals is danger - so cells turn on inflammation
2 = anti-inflammatory –> signals is no danger - so cells turn off inflammation

80
Q

What are some types of proinflammatory cytokines?

A

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

81
Q

What are some types of anti-inflammatory cytokines?

A

Interleukin 10 (IL-10)
Transforming growth factor beta (TGFβ)

82
Q

Where do cytokines travel/signal to & what does this cause?

A

-Liver = acute phase proteins released & change metabolism
-Hypothalamus = temp inc
-Bone marrow = changes haematopoesis - so more immune cells made

83
Q

What does excess of proinflammatory cytokines cause?

A

Immune-mediated inflammatory diseases (autoimmune)
-Inflammation & immune response = always active (not turned off)

84
Q

How can inflammation be made longer lasting?

A

By cytokines - as cause same responses once no histamine

85
Q

What recs do cytokines bind to?

A

Cytokine recs (are on endo cells of caps & many other places)

86
Q

What immune cells are in tissues?

A

-Dendritic
-Macrophages (to replace - monocytes move into tissues = macrophages)

87
Q

What are the 2 processes phagocytes can do?

A

-Phagocytosis takes up larger i.e., entire bacteria then break down
-Pinocytosis = takes up fluid in small endosomes
BOTH = ingesting microbes

88
Q

What are some phagocyte examples, & how are they activated?

A

-Macrophages (tissues) and activated by
pathogens & make cytokines to attract other cells
-Neutrophils, monocytes & some dendritic cells arrive at tissues from blood

89
Q

How do macrophages kill pathogens?

A

-PRR on mac binds to PAMP on pathogen
-Pathogen engulfed = phagosome
-Lysosome vesicle fuses w/ phagosome
-Enzymes - antimicrobial peptides, enzymes
& reactive oxygen species move into phagosome
-pH dec as vesicle move in
-Reactive oxygen species = damages DNA & proteins of pathogen –> so get oxidative burst enzymes digest pathogen
-Simultaneously -> mac signals & activates for other immune cells (e.g., neutrophils) by making pro-inf cytokines

90
Q

Difference between macrophage & neutrophil activity?

A

Macrophages function in tissues continually whereas neutrophils must be moved & activated from blood by cytokine to move into tissues & then undertake phagocytosis

91
Q

How do the moving immune cells ‘find’ pathogen?

A

-Move along/up chemokine gradient? - produced in tissues & moves into blood - to injury site
-Will bind to recs of immune cells

92
Q

How do neutrophils kill pathogens?

A

-Microbes are engulfed = phagosomes
-Phagosomes fuse w/ granules contain antimicrobial enzymes, proteins & peptides
-Microbes are killed by digestion & respiratory burst (as neuts make toxic O2 species)
-Pathogen killed by apoptosis (clean) or necrosis (messy)

93
Q

What is the result of necrosis?

A

= messy cell death
-Neutrophil Extracellular Traps (NETs) released – DNA covered in histone proteins & granule contents to trap microbes

94
Q

What is the neutrophil structure in terms of granules?

A

-Primary (Azurophilic) = Myeloperoxidase,
cathepsins, elastase, protease, defensins
-Secondary (Specific) = Collagenase, NAPDH oxidase & heparinase
-Tertiary (Gelatinase) = Gelatinase & lysozyme

95
Q

Why might innate immune system not kill ext pathogens?

A

-Divide too rapidly (bacteria)
-Can’t get hold of some fungi/protozoa

96
Q

What happens when ext pathogens are not killed i.e., side-effects of continued innate immunity?

A

-Keep releasing pro-inf cytokines = harmful
-Blood vs damaged so make bradykinins - inc permeability - stimulate nerves = pain
-Development to chronic inf (can = diseases)
-Toxins released by pathogens = damage cells (& use nutrients)
(ADPATIVE IMMUNITY MUST STEP IN)

97
Q

What response is needed for int pathogens?

A

Cell mediated

98
Q

How are int pathogens picked up?

A

-Toll like PRRs in endosome or NOD & RIG like PRRs in cytoplasm recognise DAMPs (due to cell damage)
-PAMPs released - activate innate immune cells
-Infected cells - flag to innate immune system (to kill)
-Pathogens will be ext at some point

99
Q

Which PRRs for viruses?

A

Mostly NOD & RIG like

100
Q

What are some PAMPs of viruses?

A

-Diff RNA & DNA
-Diff prots & sugars

101
Q

How do endosomal toll like PRRs work?

A
  1. Pathogen in endosome recognised = transmits signal to the nuc
  2. Adaptors containing TIR domains (e.g., MyD88) transmit message into cytoplasm
  3. TFs called interferon response factors (IRF) assemble and bind to DNA
  4. = instructs cells to produce new proteins
    - interferons, directing immune responses against viruses & intracellular bacteria
102
Q

What do interferon response factors (IRFs) do?

A

= Cause transcription of cytokines called interferons
-type 1 interferons = important (main innate anti-viral response)

103
Q

What are some IRF examples & what toll-like PRRs do they come from?

A

IRF-3 = from TLR 3 –> gives interferon β (IFNβ)
IRF-7 = from TLR 7,8 & 9 –> gives type 1 interferons (IFNa or IFNβ)

104
Q

How do NOD & RIG like PRRs work?

A
  1. Recognition of DAMPs & bacterial and viral PAMPs within cytoplasm transmits signal to nuc
  2. NLR aggregate to form inflammasome which
    activates & causes release of proinflammatory
    cytokines
  3. RLR aggregate & activate TFs (NFκB & IRF3) = production of new proteins e.g., type 1 interferons
105
Q

What are the 3 types of interferon?

A

-Type 1 (IFNα & IFNβ) - cytokines made by
infected cells = increase anti-viral defence
mechanisms in local cells
-Type 2 (IFNγ) – released by adaptive immune
cells to enhance innate immune functions
-Type 3 – little known but important in anti-viral
& anti-fungal responses

106
Q

What do interferons do?

A

Inc viral defences & reduce viral replication

107
Q

How to kill viruses - anti-viral responses?

A

-Turn off viral rep machinery in our cells - prevent replicating
-Kill infected own cells

108
Q

What do IFNα &IFNβ do to stop replication of viruses?

A

-Bind to IFNα & IFNβ recs = IFNAR own & local cells - auto&para-crine
-Activate genes to degrade viral RNA & stop prot syn (=capsules not made)
-Also natural killer (NK) cells recruited & activated by interferons/cytokines

109
Q

What do IFNα & IFNβ do to kill own infected cells?

A

-NK cells kill virus infected cells (& cancer cells) = apoptosis
-Interferons (cytokines) recruited NKs - acts as chemokines for them & activate NKs

110
Q

How do NK cells cause apoptosis of virus infected cells?

A

-Recognise infected cell
-Release perforin = holes in cell memb
-Put granzymes (within granules) into cell - digest cell = apoptosis

111
Q

How do NK cells know which cells to kill when none of them are foreign (own cells, just infected)?

A

Inhibitory & activating ligands on membs of cells - when there is more activating ones = signals to NKs to kill this cell (as the cell is infected)
-More activating = apoptosis (NK activated)
-More inhibitory = cell survives (NK NOT activated)

112
Q

What happens when int pathogens are not killed?

A

-NKs will kill self-cells = damaging
–> body must limit no. self-cells it is killing
-NEED ADAPTIVE - spec response

Immunology (6 decks)

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