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OPHTH Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

What structures are recognised by the innate immune system?

A

PAMPs

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2
Q

What are 4 cells involves in both innate + adaptive immune responses?

A
  1. macrophages
  2. monocytes
  3. dendritic cells
  4. mast cells
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3
Q

What are 2 humoral factors involved in both innate and adaptive immune responses?

A
  1. complement
  2. cytokines
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4
Q

What are 5 things that phagocytic cells can ingest?

A
  1. whole microorganisms
  2. insoluble particles
  3. dead host cells
  4. cell debris
  5. activated clotting factors
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5
Q

What are 4 stages of phagocytosis?

A
  1. adherence of material to cell membrane
  2. pseudopodia (finger like projections) engulf the material, membrane-bound structure called phagosome formed
  3. this fuses with lysosome to form phagolysosome, mixing contents of lysosome with the engulfed material - digest + break down material
  4. waste products released from cell
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6
Q

What are 3 things contained in lysosomes of phagocytes that can digest + brek down engulfed material?

A
  1. hydrogen peroxide
  2. oxygen-free radicals
  3. hydrolytic enzymes
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7
Q

What are the 2 key types of phagocytic cells?

A
  1. neutrophils (PMN leukocyte)
  2. macrophages
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8
Q

What is the first cell to be recruited to a site of tissue damage/infection?

A

neutrophil

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9
Q

What is the lifespan of a neutrophil like?

A

short lived

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10
Q

Where do neutrophils circulate around the body?

A

circulate in the blood then migrate into tissues

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11
Q

How many neutrophils are produced per day in a health adult and how does this change in infection?

A

10^11, can increase 10x in infection

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12
Q

Where are macrophages found?

A

dispersed throughout the tissues

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13
Q

What is a key function of macrophages, in addition to phagocytosis?

A

signal infection by release of solbule mediators

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14
Q

What process directs neutrophils towards an area of infection?

A

Chemotaxis- directed migration along chemokine concentration gradient towards area of high concentration

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15
Q

What are the stages that lead neutrophils to migrate to a site of infection?

A
  • Neutrophil rolls along normal endothelium
  • At site of damage/when antigen is presented by macrophage, a change in the nature of the endothelium
    occurs
  • Integrin activation by chemokines
  • This leads to a change in adhesion molecules into high affinity state
  • they flatten out and undergo migration through endothelium
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16
Q

How do neutrophils perform opsonisation?

A

coat pathogen with proteins to facilitate phagocytosis, opsonins are molecules that bind to antigens and phagocytes. antibody and complement function as opsonins

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17
Q

How is neutrophil binding to opsonins achieved?

A

bacterium-antibody complex -> complement activation -> Fc receptor on phagocyte binds to antibody -> CR receptor binds to complement -> oposonins bind to pathogen -> signal activation of phagocyte

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17
Q

How is neutrophil binding to opsonins achieved?

A

bacterium-antibody complex -> complement activation -> Fc receptor on phagocyte binds to antibody -> CR receptor binds to complement -> oposonins bind to pathogen -> signal activation of phagocyte

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18
Q

What may phagocytosis result in?

A

abscess formation

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19
Q

What process makes phagocytosis more effective?

A

opsonisation

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20
Q

What 2 groups can neutrophil pathogen killing mechanisms be split into?

A
  1. oxygen-independent - using enzymes or antimicrobial peptides (defensins)
  2. oxygen-dependent - respiratory burst (toxic metabolites) or reactive nitrogen intermediates
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21
Q

What are 3 examples of oxygen-independent neutrophil killing mechanisms?

A
  1. lysozyme (enzyme)
  2. hydrolytic enzymes
  3. antimicrobial peptides (defensins)
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22
Q

What are 2 types of oxygen-dependent neutrophil killing mechanisms?

A
  1. uses respiratory burst: toxic metabolites
  2. reactive nitrogen intermediates - nitric oxides
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23
Q

What are 4 toxic metabolites in the respiratory burst that is an oxygen-dependent neutrophil killing mechanism?

A
  1. superoxide anion
  2. hydrogen peroxide
  3. singlet oxygen
  4. hydroxyl radical
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24
Q

What is the result of phagocyte deficiency?

A
  • infections due to extracellular bacteria + fungi
  • bacteria: Staph aureus, Pseudomonas, E coli
  • fungi: candida, aspergillus
  • deep skin infections, impaired wound healing, poor response to abx
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25
Q

What are monocytes?

A

type of phagocyte - circulate in blood, smaller than tissue macropahges, precursor to tissue macrophages

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26
Q

What are 3 examples of pathogen recognition receptors that macrophages have?

A
  1. toll-like receptors TLR
  2. NOD-like receptors
  3. RIG-I viral genomes
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26
Q

What are 3 examples of pathogen recognition receptors that macrophages have?

A
  1. toll-like receptors TLR
  2. NOD-like receptors
  3. RIG-I viral genomes
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27
Q

What are 5 properties of cytokines?

A
  1. small secrete proteins
  2. cell-to-cell communication
  3. generally act locally
  4. powerful at low concentration
  5. short-lived
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28
Q

What are 5 types of cytokines?

A
  1. interluekins
  2. interferons
  3. chemokines
  4. growth factors
  5. cytotoxic
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29
Q

What is the function of interferons?

A

anti-viral effects

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30
Q

What is the function of growth factors in the immune system?

A

development of immune system

31
Q

What is a key type of cytotoxic cytokine?

A

TNF

32
Q

How do cytokines work?

A

transcription of gene for soluble protein in cytokine-producing cell – cytokine binds to receptor on target cell – Binding generates signal – changes in gene transcription and gene activation – biological effect

33
Q

What are 3 types of method action which cytokines may have?

A
  1. Autocrine - same cell (e.g. IL2)
  2. Paracrine - nearby cells (e.g. IFN)
  3. Endocrine - circulate to distant cell (e.g. IL6)
34
Q

What are 5 important cytokines and their functions?

A
  1. IL-1: alarm cytokine, fever
  2. TNF-alpha: alarm cytokine
  3. IL-6: acute phase proteins, fever
  4. IL-8: chemotactic for neutrophils
  5. IL-12: directs adaptive immunity, activates NK cells
35
Q

How do bacteria cause septic shock?

A

systemic infection - Bacterial endotoxins cause massive release of the TNF-alpha and IL-1 by activated macrophages = increased vascular permeability, drop in BP

36
Q

Where are dendritic cells located?

A

likely sites of infection - skin, near mucosal epithelia

37
Q

What is meant by the triggered enzyme cascade system of complement?

A

initially inactive precursor enzymes - as a few are activated, they catalyse the cleaving of secondary components. rapid, highly amplified response

38
Q

What 3 things produce components of complement?

A
  1. Liver (main site)
  2. Monocytes
  3. Macrophages
39
Q

What are the 3 routes of activation of the complement cascade?

A
  1. classical pathway: antigen-antibody complexes
  2. alternative pathway: pathogen surfaces
  3. lectin pathway: antibody independent activation of classical pathway by lectins binding to carbohydrates on pathogens (MBL + CRP)
40
Q

Where do the classical + alternative pathways converge?

A

C3 - leads to final common pathway resulting in formation of membrane attack complex (MAC) -
Hydrolysis of C3 by C3 convertase

41
Q

What 4 types of immunoglobulin can activate the classical complement pathway?

A
  1. IgM
  2. IgG1
  3. IgG2
  4. IgG3
    (not IgA/E/D)
42
Q

Which immunoglobulin is most efficient at activating the complement cascade via the classical route?

A

IgM

43
Q

How many plasma proteins circulate that contribute to the complement cascade and in what form is this?

A

9 - inactive form

44
Q

What is a key property of the complement proteins?

A

heat labile

45
Q

What are 5 constituents of bacterial cell wall constituents which can activate the alternative complement pathway?

A
  1. LPS
  2. techoic acid
  3. viruses
  4. dextran
  5. IgA (occasionally)
46
Q

How does activation of the lectin complement pathway work?

A

initiated by binding of serum lectin to mannose-containing proteins or to CHO on the bacteria or viruses

47
Q

What is the major amplification step of all 3 complement pathways?

A

Hydrolysis of C3 by C3 convertase

48
Q

Which 2 organisms is the memrane attack complex particularly good at lysing?

A
  1. Enveloped viruses
  2. Gram-negative bacteria
    lyses broad spectrum of organisms
49
Q

Which organisms is the MAC bad at lysing and why?

A

gram positive bacteria - thick layer of peptidoglycan in their cell wall or due to capsular sialic acid

50
Q

What is the classical infection people are affected by who have terminal complement deficiencies (C5-9)?

A

Neisseria spp

51
Q

What is the principle opsonin of the complement cascade (common end pathway)?

A

C3b

52
Q

What are 3 ways that control mechanisms of the complement pathway are achieved?

A
  1. lability of components - short half life
  2. dilution of components in biological fluids
  3. specific regulatory proteins - circulating/soluble + membrane bound
53
Q

What are 4 examples of circulating/soluble specific regulatory proteins that control complement cascade?

A
  1. C1-inhibitor
  2. Factor I
  3. Factor H
  4. C4 binding protein
54
Q

What are 2 examples of membrane bound specific regulatory proteins that control complement cascade?

A
  1. CD59 - interferes with MAC insertion
  2. DAF - competes for C4b
55
Q

What are 7 key functions of the complement pathway?

A
  1. lysis
  2. opsonisation
  3. anaphylatoxins - C3b, C4b, C5a
  4. mediate degranulation of mast cells
  5. viral neutralisation
  6. promotes phagocytic clearance of immune complexes
  7. aiding in antigen presentation
56
Q

How does the complement cascade aid in opsonisation?

A

Complement components (e.g., C3b, C5a and C4b) are recognised by specific receptors on phagocytes and enhance phagocytosis of the coated pathogen

57
Q

Which complement components act as anaphylatoxins and how?

A
  • C3a, C4a and C5a = induce smooth muscle contraction and increase vascular permeability
58
Q

Which complement components mediate mast cell degranulation?

A

C3a + C5a

59
Q

How can complement play a part in neutralising virus?

A

coating the virus and blocking their attachment to cellular receptors

60
Q

How does complement promote humoral immunity?

A

by aiding in antigen presentation to B cells in germinal centres, and by binding to a receptor on B cells which acts as a co-stimulator

61
Q

What are 2 sites of mast cells?

A
  1. mucosal - lung
  2. connective tissue - skin and peritoneal cavity, near blood vessels
62
Q

Which complement products are degranulated by mast cells?

A

anaphylatoxins –> vasodilatation, vascular permeability

63
Q

What are 3 key features of the local acute inflammatory response?

A
  1. invasion of pathogens
  2. complement activation
  3. endothelial damage
64
Q

What are the consequences of the invasion of pathgens in the local acute inflammatory response?

A
  • recognition by macrophages
  • phagocytosis
  • release of soluble cytokines + chemokines
  • Diapedesis and Chemotaxis (slowing down of neutrophils in blood vessels and migration towards site of infection)
65
Q

What are the consequences of complement activation in the local acute inflammatory respose?

A
  • mast cell degranulates
  • release of pro-inflammatory fragments + histamines
66
Q

What are the consequences of endothelial damage in the local acte inflammatory response?

A
  • change in nature of endothelium
  • signals site of infectionto neutrophils
66
Q

What are the consequences of endothelial damage in the local acte inflammatory response?

A
  • change in nature of endothelium
  • signals site of infectionto neutrophils
67
Q

How long after the local inflammatory response may the systemic ‘acute phase’ response start?

A

1-2 days

68
Q

What are 4 key acute phase proteins?

A
  1. CRP - activates complement
  2. Mannan binding lectin - opsonin for monocytes, activates complement
  3. Complement
  4. Fibrinogen - clotting
69
Q

What are 3 things indicating the importance of cytokines?

A
  1. signal liver - produce acute phase proteins
  2. signal bone marrow - CSF by stromal cells and marophages, increase WBC production
  3. signal hypothalamus - prostaglandin production, fever, pituitary gland + adrenal cortex - corticosteroids
70
Q

What type of cells are natural killer cells?

A

large granulated lymphocytes

71
Q

What are the 2 key types of cytokines produced by NK cells?

A
  1. IFN-gamma
  2. TNF-alpha
72
Q

Do NK cells have an antigen specific receptor?

A

no

73
Q

What is a key role of the receptors on the surface of NK cells?

A

bind to antibody coated cells - ADCC - antibody dependent cell-mediated cytotoxicity

74
Q

Which type of virus are NK cells particular important in defence against?

A

herpes

75
Q

What processes prevent NK cells from killing non-infected self cells?

A

ligation of inhibitory NK receptors to inhibit target cell killing due to recognition of lack of MHC molecules

76
Q

Which complement component is present in the highest concentration in serum?

A

C3

OPHTH Immunology (8 decks)

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