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Year 2 - T3 Theme 1 > L2 - Innate immunity 1: soluble effectors > Flashcards

L2 - Innate immunity 1: soluble effectors Flashcards

1
Q

What is innate immunity

A
  • 1st line of defence against infection
  • Present at birth and passed down genetically
  • Occurs within minutes of pathogen recognition
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2
Q

Characteristics of innate immunity

A
  • Specifically inherited in the genome
  • Expressed by all cells of a particular type (eg. macrophages - variable)
  • Triggers immediate response
  • Recognises broad classes of pathogens
  • Interacts with a range of molecular structures of a given type
  • Able to discriminate between even closely related molecular structures
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3
Q

Characteristics of adaptive immunity

A
  • Encoded in multiple gene segments
  • Requires gene rearrangement
  • Clonal distribution
  • Able to discriminate even closely related molecular structures
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4
Q

Physical innate barriers to infection

A
  • Skin
  • Respiratory tract
  • GI tract
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5
Q

Soluble innate barriers to infection

A
  • Complement
  • Defensins
  • Collectins
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6
Q

Induced innate barriers to infection

A
  • Innate immune cells
  • Pattern recognition
  • Receptors (PRRs)
  • Interferons
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7
Q

Examples of mechanical anatomical barriers to infection - Skin

A
  • Epithelial cells joined by tight junctions

- Longitudinal flow of air or fluid

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8
Q

Examples of mechanical anatomical barriers to infection - gut

A
  • Epithelial cells joined by tight junctions

- Longitudinal flow of air or fluid

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9
Q

Examples of mechanical anatomical barriers to infection - lungs

A
  • Epithelial cells joined by tight junctions

- Movement of mucus by cilia

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10
Q

Examples of mechanical anatomical barriers to infection - eyes/nose/oral cavity

A
  • Tears

- Nasal cilia

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11
Q

Examples of chemical anatomical barriers to infection - skin

A
  • Fatty acids

- Antimicrobial peptides

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12
Q

Examples of chemical anatomical barriers to infection - gut

A
  • Low pH
  • Antimicrobial enzymes
  • Antimicrobial peptides
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13
Q

Examples of chemical anatomical barriers to infection - lungs

A
  • Pulmonary surfactant

- Antimicrobial peptides

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14
Q

Examples of chemical anatomical chemical barriers to infection - eyes/nose/oral cavity

A
  • Antimicrobial enzymes in tears and saliva

- Antimicrobial peptides

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15
Q

Response to tissue damage

A

1) Tissue damage causes release of vasoactive and chemotactic factors that trigger a local increase in blood flow and capillary permeability
2) Permeable capillaries allow an influx of fluid(exudate) and cells
3) Phagocytes migrate to site of inflammation (chemotaxis)
4) Phagocytes and antibacterial exudate destroy bacteria

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16
Q

Examples of soluble innate immune molecules

A
  • Enzymes such as lysozyme
  • Antimicrobial peptides
  • Collectins, ficolins and pentraxins
  • Complement components
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17
Q

Function of enzymes such as lysozymes

A
  • Disrupts bacterial cell walls; found in blood and tears
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18
Q

Function of antimicrobial peptides

A
  • Disrupt microbial membranes
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19
Q

Function of colelctins, ficolins and pentraxins

A
  • Bind to pathogens targeting them for phagocytosis and activate complement
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20
Q

Functions of complement components

A
  • Lyse bacteria, opsonise bacteria, induce inflammation
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21
Q

What are lysozymes released by

A
  • Phagocytes and paneth cells from the small intestine
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22
Q

What are lysozymes most effective against

A
  • Most effective against gram-positive bacteria

- Cleaves the bond between the alternating sugars that make up peptidoglycans which disrupt them

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23
Q

Examples of antimicrobial peptides

A
  • Histatins
  • Defensins
  • Cathelicidins
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24
Q

Where are histatins produced

A
  • Produced in the oral cavity
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25
Q

What are histatins active against

A
  • Pathogenic fungi, eg. candida albicans
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26
Q

What are cathelicidins active against

A
  • LL-37 broad-spectrum antimicrobial activity against both gram-negative and gram-positive bacteria
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27
Q

Where are antimicrobial peptides found

A
  • Cover epithelial surfaces, found in saliva
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28
Q

What are antimicrobial peptides secreted by

A
  • Neutrophils, epithelial cells and paneth cells in the crypts of the small intestine
29
Q

Actions of antimicrobial peptides

A
  • Kill bacteria in minutes, by disrupting the membrane
  • Also attack fungi, viruses (influenza and herpes virus)
  • Inhibit DNA and RNA synthesis
30
Q

Classes of defensins

A

Two classes - alpha and beta defensins

31
Q

Features of defensins

A
  • 35-40 aa amphipathic peptides which means they have both hydrophilic and hydrophobic regions on their cell surface
  • Disulphide bonds stabilise the structure to have a positively charged region separated from a hydrophobic region
  • Disrupt microbial membranes but not that of the host
32
Q

Features of collectins

A
  • Have globular lectin like heads that bind bacterial cell surface sugars
  • Sialic acid hides mannose antigens on host cells
33
Q

Features of ficolins

A
  • Recognise acylated compounds(COCH3) such as n-acetylglucosamine, a monosaccharide found in bacterial cell walls
34
Q

Features of pentraxins

A
  • Are cyclic multimeric proteins found in the plasma
35
Q

What is used as a clinical measure of inflammation

A
  • C-reactive protein (CRP) is used as a clinical measure of inflammation
36
Q

Actions of collectins, ficolins and pentraxins

A
  • Soluble pattern recognition receptors
  • Act as opsonins that bing to pathogens and infected cells targeting them for phagocytosis
  • Activate complement through the classical pathway/lectin pathway
37
Q

Complement pathways

A
  • Classical
  • Lectin
  • Alternative
38
Q

Features of the complement system

A
  • Series of over 30 proteins that constantly circulate in blood and fluids that bathe the body tissues
  • When they detect presence of foreign material, they initiate a cascade of reactions that amplify the signal
39
Q

Classical pathway

A
  • Antigen:antibody complexes (pathogen surfaces) –> C1q, C1r, C1s, C4, C2 –> C3 convertase
40
Q

Lectin pathway

A
  • Mannose-binding lectin or ficolin binds carbohydrate on pathogen surfaces –> MBL/ficolin, MASP-2, C4, C2 –> C3 convertase
41
Q

Alternative pathway

A
  • Pathogen surfaces –> C3, B and D –> C3 convertase
42
Q

Products of C3 convertase

A
  • C3a, C5a, C3b–> terminal complement components C5b, C6, C7, C8, C9
43
Q

Effects of C3a, C5a

A
  • Peptide mediators of inflammation, phagocyte recruitment
44
Q

Effect of C3b

A

C3b –> binds to complement receptors on phagocytes –> opsonization of pathogens + removal of immune complexes

45
Q

Effects of terminal complement of components

A
  • Membrane attack complex

- Lysis of certain pathogens and cells

46
Q

What happens when the complement system is activated

A
  • When activated, cooperate with other host defense systems to generate inflammation and rapidly remove the pathogen
47
Q

Where are proteins in the complement system made

A
  • Most made by the liver but also produced by monocytes, macrophages and epithelial cells of the intestine and urinary tract
48
Q

Features of complement components

A
  • Circulate as a pro-form (inactive) in the blood
  • Numbered in the order they were discovered, not in the order they are activated
  • Some have proteolytic enzymatic activity
  • On activation, they split into a small and large fragments triggering an amplification cascade
49
Q

Effects mediated by complement components

A
  • Lysis
  • Opsonisation
  • Activation of inflammatory response
  • Clearance of immune complexes
50
Q

What is the classical pathway initiated by

A
  • Initiated by C1 activation
51
Q

What is C1

A
  • C1 is a complex of three proteins: C1q, C1r and C1s
52
Q

What is the structure of C1 dominated by

A
  • The structure of C1 is dominated by C1q

- A large molecule of 18 polypeptides that form six collagen like triple helix structures

53
Q

What activates the classical pathway

A
  • Triggered when C1 binds to the Fc region of an antibody-antigen complex
  • C1 must bind at least 2 FC domains
54
Q

Which antibody is most efficient at activating the classical pathway

A
  • IgM is the most efficient at activating complement as it has 5 Fc domains
  • IgG1 and IgG3, and to a lesser extent IgG2 can also activate complement when close together bound to antigen
55
Q

Why can’t serum IgM bind C1

A
  • Serum IgM cannot bind C1 as it has a planar conformation, the shape changes on binding antigen to reveal binding sites for C1q
56
Q

Process of classical pathway amplification

A
  • Binding C1q with the Fc domain causes a conformational change in C1r
  • C1s is cleaved and can activate C2 and C4 splitting into their large and small fragments
  • C3 convertase (C4b2a) can then activate over 200 C3 molecules producing a massive amplification of the signal
  • C4b, C2a and C3b fragments form the C5 convertase that activates C5 leading to the membrane attack complex
57
Q

What is the lectin pathway activated by

A
  • Antibody independent, activated by ficolins and mannose binding lectin (MBL)
58
Q

Process of lectin pathway activation

A
  • MBL binds mannose residues on carbohydrates and glycoproteins on bacteria and some viruses
  • Similar downstream mechanism to the classical pathway
  • Upon binding, MBL forms a complex with MASP-1 and MASP-2 (serine proteases)
  • Active complex cleaves C2 and C4
59
Q

Alternative pathway

A
  • C3 spontaneous hydrolyses into C3a and C3b
  • C3b binds to a cell membrane and factor B, making it susceptible to cleavage by factor D to Bb
  • C3bBb has a half-life of 5 mins, unless it binds the serum protein properdin, which extends it half-life to 30 mins by protecting it from proteases
  • C3b,Bb can hydrolyse more C3 creating more C3b which can amplify the signal
60
Q

Action of the membrane attack complex

A
  • MAC forms a pore that inserts into the membrane allowing diffusion of ions and small molecules, water moves into the cell killing it
  • Human cells have soluble and cell surface associated proteins that prevent MAC formation
61
Q

Action of C1 inhibitor

A
  • C1 inhibitor is a soluble protein that prevents C1-activating C4 and C2
62
Q

What is deficient in hereditary angioedema

A
  • C1 inhibitor deficiency

- Classical complement cascade easily activated but can be treated with an injection of C1 inhibitor

63
Q

What do patients with complement component deficiency experience

A
  • Recurrent infections
64
Q

What does MBL deficiency cause

A
  • MBL deficiency causes serious pyogenic infections in neonates and children
65
Q

Most severe complement deficiency

A
  • C3 deficiency is the most severe leading to successive severe infections
66
Q

What are patients deficient of C8 prone to

A
  • Patients deficient of C8 are prone to infection with neisseria meningitis
67
Q

What can people deficient of C4 develop

A
  • 90% of people deficient for C4 develop the autoimmune disease systemic lupus erythematosus (SLE)
68
Q

Implications of C4 deficiency

A
  • C4 deficiency means less C3b(C4b2a is C3 convertase)

- C3b bound to immune complexes binds to CR1 on erythrocytes which transports them to phagocytes in the liver and spleen

69
Q

How do phagocytes recognise immune complexes

A
  • Phagocytes recognise the immune complexes via their Fc receptors and engulf them

Year 2 - T3 Theme 1 (15 decks)

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