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Innate Immunity Flashcards

1
Q

What are the 3 traits of innate and adaptive immunity? (hint - specificity, prior, time)

A

Innate:
- Broad specificity
- Not affected by prior contact; No memory
- Immediate/rapid response (hours)

Adaptive:
- Highly specific
- Enhanced by prior contact; Memory
- Slow response (days-weeks)

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2
Q

What components make up the innate immune system? (4 things) Give examples

A

Barriers (physical, chemical)
Soluble proteins (complement, interferons etc.)
Local and systemic responses (inflammation, fever)
Leukocytes (Phagocytes, NK cells)

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3
Q

What components make up the adaptive immune system? (4 things) (hint - memory, types of immunity)

A

B and T lymphocytes
B cells respond by secreting soluble antibodies - Humoral immunity
T cells develop into cytotoxic T cells or helper T cells - Cell mediated immunity
Both B and T cells can develop into memory cells

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4
Q

What part of the immune system derives from pluripotent stem cells?
What are the 2 main lineages and what part of the immune system are they involved in? (hint - Mye, Lym)

A

Leukocytes

Myeloid lineage - Innate
Lymphoid lineage - Humoral

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5
Q

How does the body recognise function (i.e. whether a cell is innate and adaptive)?

A

Innate - Pattern Recognition Receptors (PRRs) that recognise Pathogen Associated Molecular Patterns (PAMPs) on cells of the innate immune system

Adaptive - B and T lymphocytes express specific antigen receptors

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6
Q

What do PRRs recognise?
What are the traits of these? (3 traits)

A

PAMPs/MAMPs

Unique to microbes
Conserved
Essential for microbe survival

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7
Q

What is clonal selection?
What happens to ‘self’ recognising lymphocytes?

A

Antigen binds antibody being presented on certain B lymphocyte
Activates B lymphocyte causing it to proliferate and produce more of that antibody

Lymphocytes that recognise ‘self’ are deleted early in development

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8
Q

The immune system aims to maximise host defences while minimising damage to host tissues
What are the traits of innate immunity that link to this? (hint - number, distinguishing, activation, targeting)

A

Innate:
- Small number of inherited PRRs recognise MAMPS unique to microbes
- Good at distinguishing between self/non-self
- Non-clonal activation
- Potential for collateral damage to self (immunopathology)

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9
Q

The immune system aims to maximise host defences while minimising damage to host tissues
What are the traits of adaptive immunity that link to this? (hint - number, distinguishing, activation, targeting)

A

Adaptive:
- ‘Infinite’ number of randomly generated antigen receptors
- Cannot reliably distinguish between self/non-self or between harmful/innocuous material
- Clonal activation
- Targets immune response specifically towards infection, sparing uninfected tissues

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10
Q

How are innate and adaptive immunity linked?

A

Innate immune system activates and directs adaptive responses
Adaptive immune system can control and focus innate immunity

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11
Q

What occurs in primary and secondary lymphoid tissue?

A

Primary - Lymphocytes reach maturity and acquire their specific receptors

Secondary - Mature ‘naïve’ lymphocytes are stimulated by antigen

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12
Q

How do lymphocytes meet antigen?

A

Dendritic cells and macorphages present antigen via uptake and MHCII expression
These then go to the secondary lymhpid tissue where they present them to lymphocytes

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13
Q

Adaptive immunity takes ~4-6 days to develop. Why is innate immunity then essential?

A

Critical in controlling infections before this

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14
Q

Explain microbiology as a barrier
What exposed tissues have this is a barrier?

A

Commensals help deter pathogenic bacteria

Almost all have commensals growing on them

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15
Q

What do all mechanical barriers involve?
Give examples of mechanical barriers and what they use

A

Epithelial cells joined by tight junctions

Lungs have cilia to move mucous
Urogenital tract has the flow of urine

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16
Q

How is keratinised skin a barrier?
What do keratinocytes produce and what does this do? (2 things)
How does skin shedding and commensal growth help?

A

Generally impermeable

Keratin; Strong and bacteria struggle to grow on this
Sebum; Contains fatty acids

Methods to get rid of and prevent bacterial growth

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17
Q

How do the gut and urogenital tract act as a chemical barrier?

A

Gut - Low pH enzymes in stomach acid to destroy bacteria
Urogenital tract - Low pH (vagina) urine

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18
Q

How do mucous membranes work with cilia?

A

Mucins are secreted in the respiratory tract to trap microbe and cilia direct mucous towards stomach acid

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19
Q

What are preformed mediators? (hint - broad)
Give an example; Why is it more effective against gram positive bacteria?

A

Proteins/peptides with broad specificity that damage pathogens, induce inflammation or help recruit and activate innate immune cells

Lysozymes present in secretions (tears, saliva, mucous etc.)
Breaks a bond in peptidoglycan; Gram +ve have more peptidoglycan and no outer membrane

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20
Q

Antimicrobial peptides are a type of pre-formed mediators. Give an example, where its produced and what it does

A

Defensins

Produced by many epithelial cells and neutrophils

Cationic, disrupt lipid bilayers in bacteria, fungi and enveloped viruses

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21
Q

What is complement and what does it consist of?
It is normally inert, but when is it activated and what does this trigger?

A

Heat-sensitive substance that “complements” antibodies in killing bacteria
- >20 soluble proteins found in blood and other body fluids

“Activated” by presence of pathogens or antibody bound to pathogen
This triggers an activation cascade

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22
Q

What does complement activation do early in infection?

A

Provides protection early in infection in the absence of antibodies

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23
Q

Which part of complement is essential for all pathways of activation and why?
- What is this executed by?

A

C3

Central event of complement activation is cleavage of C3; Executed by C3 convertase in all pathways

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24
Q

Why is C3 –> C3b (larger) + C3a important in complement activation? (hint - protease)

A

Cleavage of C3 exposes a reactive thioester (protease) in C3b; This binds covalently to adjacent proteins/carbohydrates e.g. on pathogen surface

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25
What are the 3 pathways of complement activation?
Classical pathway – Antibody binding Alternative pathway Mannose-binding lectin (MBL) pathway – MBL binds mannose on pathogen surface - Lectin – Binds tightly to carbohydrates
26
How do the classical and MBL pathway produce C3 convertase?
C3 convertase = C4b-C2a complex Cleavage of C4 and C2 by C1 and MASP2, respectively
27
How does alternative pathway produce C3 convertase? (hint - LPS, factor B, D and P) - There are more steps to this pathway
C3 convertase = C3b-Bb complex Some C3b is generated spontaneously in body fluids by a “tickover” mechanism If C3b generated binds to LPS on a pathogen surface, factor B binds Factor B is then cleaved by factor D to produce C3b-Bb complex C3b-Bb convertase is stabilised by factor P
28
How can classical/MBL pathway link with alternative pathway?
C3b generated by the classical or MBL pathway can also bind factor B
29
What do C5a and C3a do and what can they be called? Give more detail (hint - receptors, blood vessels, mast cells)
Recruit phagocytes and induce inflammation - a.k.a Chemoattractants, anaphylatoxins Phagocytes have C5a and C3a receptors and undergo chemotaxis in response to C5a/C3a peptide C5a/C3a act on local blood vessels, increasing blood flow, permeability and phagocyte adhesion C5a/C3a binding to C5a/C3a receptors on mast cells induces release of inflammatory mediators
30
What does C3b promote and what does this facilitate?
C3b coats pathogens (opsonisation), causing them to be recognised by phagocytes with C3b receptors This facilitates binding and phagocytosis
31
What does C5b - C9 form and lead to? (hint - MAC) How? What organisms is this important in killing?
Forms the membrane attack complex which leads to lysis This causes C9 polymerisation which forms a pore in the membrane Important for killing gram -ve bacteria
32
Why is complement referred to as a double-edged sword? How is regulation achieved? (2 ways)
Regulation needed to prevent damage to host Components rapidly hydrolysed in fluid phase to deactivate them Soluble and membrane bound regulatory proteins to help regulate
33
Give 4 examples of regulatory proteins that regulate complement Give 2 examples of where deficiencies in these inhibitors increase risk of disease
Factor H competes with factor B Factor I protease cleaves C3b CD59 on host cells binds C9, preventing MAC formation Decay-accelerating factor (on host cells) interferes with the formation of C3 and C5 convertases Age-related macular degeneration (lack Factor H) Increased risk of some infections and autoimmune diseases (Factor I deficiency)
34
What infections are complement activation particularly important in?
Extracellular bacterial and fungal infections
35
How does complement interact with adaptive immune system?
Classical Pathway Aids clearance of immune complexes (antigen:antibody) Role in activating B and T cells
36
What are polymorphonuclear granulocytes? Give examples (hint - very common white blood cells)
Immune cell that has granules (small particles) with enzymes that are released during infections, allergic reactions, and asthma - Basophils - Eosinophils - Neutrophils
37
What are neutrophils and what receptors do they have? What is a NET and what does it allow?
Most common leukocyte Receptors for C3b, IgG and IgA NET (neutrophil extracellular trap) consists of DNA and antimicrobials Allows neutrophils to kill extracellular pathogens while minimizing damage to the host cells
38
What are eosinophils and what receptors do they have? (hint - allergy) What do they release and defend against?
Leukocytes that are few in number in the blood Receptors for C3b, IgG, IgA - IgE with role in allergy (especially asthma) Release toxic proteins and free radicals Defence against multicellular parasites
39
What are basophils and what receptors do they have? What do they release and defend against?
Leukocytes very few in number in the blood Receptors for C3a, C5a, IgE Release heparin and histamine Defence against parasites, role in allergy (IgE)
40
Where are mast cells restricted to and what receptors do they have? What do they release and defend against? (hint - sentinel)
Restricted to tissues – protect mucosal surfaces. Receptors for C3a, C5a, IgE Release histamine “Sentinel” cells, defence against parasites, role in allergy
41
Difference between monocytes and macrophages?
Monocytes are in blood; Macrophages are tissue resident Macrophages derive from monocytes during infection (when monocytes move from blood to tissue)
42
What do different tissues have? (hint - macrophages) Give traits for lung and brain macrophages (hint - sentinel)
Different tissues have different resident macrophages e.g. alveolar macrophages (lung), microglia (brain) - Long-lived - Act as “sentinel” cells – Often the first to detect infections - Can present antigen to T lymphocytes
43
What do dendritic cells do? What are they specialised for and what do they express highly?
Digest foreign material and display fragments on their cell surface Specialised for presenting antigen to T cells Constitutively express high levels of Major Histocompatibility Type II (MHCII) proteins
44
What 4 cell types perform phagocytosis? How do healthy self-cells prevent phagocytosis by these cells?
Neutrophils Monocytes Macrophages Dendritic cells Healthy self-cells express CD47 protein which is recognised by phagocytes
45
What is the sequence of events during phagocytosis? (4 steps)
1. Bacterium binds surface of phagocytic cell; Antibody or complement can aid binding 2. Phagocyte pseudopods extend and engulf the organism 3. Invagination of phagocyte membrane traps the organism within a phagosome 4. A lysosome fuses and deposits enzymes into the phagosome; Enzymes cleave macromolecules and generate reactive O2 species, destroying the organism
46
What bactericidal agents exist in the phagosome?
Acidic (low) pH; Can also be bacteriostatic Toxic O2-derived products Toxic nitrogen oxides Antimicrobial peptides Enzymes e.g. lysozymes Competitors e.g. lactoferrin binds Fe, depriving bacteria of Fe
47
What happens in O2-dependent killing when phagosomes come into contact with pathogen? (hint - 3 enzymes)
NADPH oxidase in the phagosome membrane is activated, converting O2 to superoxide ion O2(1-) Superoxide dismutase converts the superoxide to hydrogen peroxide Peroxidase enzymes and iron convert hydrogen peroxide to hypochlorite ion and hydroxyl radicals All these damage bacterial DNA, proteins and membrane
48
What do Natural Killer (NK) cells recognise and kill? (hint - MHC) What types of infections are they important in and what receptors do they have? (hint - until adaptive)
Recognise "altered self", specifically self Major histocompatibility Type I (MHCI) proteins Kill infected cells Important in viral and some intracellular bacterial infections, until adaptive immunity is triggered Receptors for IgG
49
Pattern Recognition Receptors (PRR) recognise relatively invariant structures like MAMPs and DAMPs. What are these?
MAMPs - Critical for survival/function of pathogens - Conserved Damage-associated molecular patterns (DAMPs) - Host components released during injury and cell damage
50
Give examples of MAMPs for bacteria (+ve and -ve), virus, fungi and protozoa
Bacteria - Gram +ve; Lipoteichoic acids - Gram -ve; Lipopolysaccharides (LPS) Fungi - Chitin Viruses - dsRNA Protozoa - Mannose-rich glycans
51
Give 2 examples of DAMPs and where they come from
Uric acid - Sign of kidney damage Phosphatidylserine - Normally intracellular but is exposed during apoptosis
52
Give an example for each class of PRR (soluble, membrane and cytoplasmic receptor)
Soluble - Mannose-binding lectin Membrane - Lectin receptor - Toll-like receptor Cytoplasmic - NOD-like receptor (NLR)
53
How does PRR binding to MAMPs initiate macrophage phagocytosis? Give 2 binding examples
PRR recognises relevant MAMP - e.g. Macrophage mannose receptor recognises mannose - e.g. CD14 recognises LPS Macrophage then engulfs MAMP (and pathogen) and releases chemokines and cytokines
54
How does PRR binding to MAMP initiate chemotaxis or signalling? Give 1 example for each
Chemoattractants released which are recognised by chemotactic receptors Toll-like receptors (TLRs) signal the presence of microbial components
55
How many human TLRs are there recognising distinct MAMPs and where can they be? How does TLR activation and signalling work? (hint - dim...) TLR structure?
10 TLRs either on cell-surface or endosome Ligand bind and induced dimerisation of TLR which induces signalling Extracellular domain of TLR3 has horseshoe shape with inner surface β-sheet structure forming ligand binding domain
56
What are NOD-like receptors (NLR)? What do they signal and trigger? (hint - inflam)
Large group of cytoplasmic receptors that recognise bacterial components e.g. peptidoglycan Signal expression of pro-inflammatory cytokines Trigger assembly of inflammasomes
57
What is the inflammasome and its main purpose? What is the process?
Multi subunit complex that cleaves inactive cytokine precursors in order to limit inflammation Active NLRs signal either cytokine transcription or inflammasome formation Inflammasome binds protease to cleave procytokines into active cytokines for release
58
What is inflammation and why is it a critical local response to infection?
Release of Chemoattractants to attract phagocytes, and inflammatory mediators to increase blood flow and vascular permeability so phagocytes can gain access to microbes in tissues
59
Inflammation ensures that immune cells, defence molecules, coagulation factors etc. reach the site of infection or tissue damage What are the 5 signs of inflammation?
Redness, swelling, heat and pain Release of inflammatory mediators Dilation of local blood vessels Increased permeability and blood flow Immune cell migration into inflammatory site
60
Inflammatory mediators are produced by sentinel cells, tissue damage and microbes. What are the 5 types? Give 1 example for each
Lipid mediators - Prostaglandins Vasoactive amines - Histamine Chemoattractants - fmet-leu-phe Complement proteins - C5a Cytokines -TNF
61
What is acute inflammation?
Movement of white blood cells from blood vessels into the tissues; Also known as “extravasation”
62
What are the "hormones" of the immune response? What do they do? (hint - regulate) What do they act on and how tightly are they regulated?
Cytokines Regulate immune responses by changing cell behaviour of gene expression Act on cells bearing specific cytokine receptors Expression of cytokines and their receptors is tightly regulated
63
What are the 4 families of cytokine and their function?
IL-1 family - Most produced as inactive precursors that must be cleaved by inflammasomes; Important in inflammation Interferons - Involved in responses to viruses TNF family - Many are TM proteins but can be shed; Important in inflammation Chemokines - Involved in cell movement
64
Similarities within a cytokine family?
Cytokine receptors for the various subfamilies tend to have similar structure and to signal in a similar way
65
Give an example of a local and systemic effect induced by any cytokine released during macrophage activation (hint - TNFα)
TNFα Local - Activates vascular endothelium and increases vascular permeability, which leads to increased entry of IgG, complement, and cells to tissues and increased fluid drainage to lymph nodes Systemic - Fever - Mobilisation of metabolites - Shock - Toxic
66
Why is TNF and TNFR expression tightly regulated? How is TNF made and what stimuli are potent? How is TNFR activated and what are its 2 pathways?
Toxic unless in very low doses Made by macrophages and LPS is a potent stimulus TNF trimer cross-links 3 receptors, inducing signalling Cell stimulation and apoptosis pathways
67
What are TNFs local effects and why? (3 effects)
Increased blood flow, capillary permeability - Influx of fluid, cells and proteins into infected tissue Influx of platelets - Clotting in capillaries helps prevent spread of infection Fluid from the capillaries enters tissues - Increased drainage to lymph nodes - Stimulation of adaptive immunity
68
What are TNFs systemic effects (low conc.)? (hint - temperature) When cause TNF cause damage?
Causes fever by acting on hypothalamus to raise temperature to inhibit bacterial/viral growth and for optimum T and B lymphocyte activation Inappropriate production of TNF e.g. in autoimmune disease, can cause tissue damage through chronic inflammation
69
What are TNFs systemic effects (high conc.)? (3 effects)
Hypotension (low blood pressure) Disseminated (widespread) clot formation which can cause organ damage Consumption of clotting factors can cause greater spread of infection - Septic shock
70
What was the first cytokine used to treat rheumatoid arthritis? Drugs which target this are the most successful in treating what?
TNF Treating chronic inflammation and autoimmune disease
71
Viral infection induces production of interferons. What do they do?
Interfere with viral replication and alert immune system
72
What do Type I interferons do? (3 main things) (hint - translation, MHCI, recruit)
Induce expression of endoribonuclease that degrades viral RNA and protein kinase that phosphorylates eukaryotic initiation factor 2, inhibiting protein translation Increases MHCI expression for greater antigen presentation to cytotoxic T cells, so infected cells are more easily recognised and killed Induce chemokines to recruit lymphocytes
73
Give an example of 2 Type I interferons and a cell type specialised for their production
IFNα, IFNβ Dendritic cells - Express high levels of interferons - Normal cells also produce interferons just not as many
74
What do Type II interferons do? Give an example of one and a cell that makes it?
Primary role in modulating adaptive immunity by increasing expression of MHCI and MHCII IFN-γ made by T helper cells activates macrophages in responses to intracellular pathogens
75
What is a cytokine storm? When may this occur? Treatments?
An exaggerated immune response to infection with highly elevated levels of pro-inflammatory cytokines e.g. TNF, IL-1β, IL-6 May occur in sepsis, toxic shock syndrome, severe burns Cytokine/Cytokine receptor inhibitors Corticosteroids
76
How do innate and adaptive immunity interact?
Innate responses initiate adaptive responses (antigen presentation) and different cytokines steer adaptive responses by activating different T cell subsets, promoting the production of different antibody classes Adaptive responses use elements of innate immunity to eliminate pathogens e.g. classical pathway of complement, activation of macrophages by T cell cytokines, antibodies can help NK cells recognise infected cells, mast cells to respond to parasites

Molecular Immunology (5 decks)

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