Lecture 2 - Innate Immunity Flashcards

1
Q

what antimicrobial factors are produced to protect against microbes?

A

lysozyme, lactic and fatty acids

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2
Q

how does the GI tract fight microbes?

A

has digestive enzymes to kill microbes

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3
Q

how does the liver contribute to fighting infection?

A

carries out oxidisation of xenobiotics, detoxification and synthesis of defence factors

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4
Q

what is NETosis?

A

neutrophil extracellular traps

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5
Q

what molecules are linked to the activation of an acute phase reaction?

A

C-reactive protein for inflammation, serum amyloid A and mannose binding lectin

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6
Q

what type of antibody is also associated with innate response?

A

IgM as not specific and no memory cells produced due to T cell independent action

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7
Q

what are the antimicrobial peptides?

A

alpha defensins, cathelicidins, lactoferrin and dermicidin

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8
Q

where does natural cytotoxicity come from?

A

due to innate lymphoid cells, NK cells, and natural cytostasis induced by interferons

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9
Q

what defences are involved when a pathogen attaches to epithelium?

A

normal flora, chemicals such as fatty acids and phagocytes under epithelial cells

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10
Q

what defences are involved when a pathogen penetrates epithelial cells?

A

antimicrobial proteins and peptides and phagocytes and complement produced to destroy the microbe

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11
Q

what defences are involved in local infection of tissues?

A

fibrin localises the infection and stops it from entering the blood stream, complement and cytokines produced, dendritic cells go to lymph nodes and blood clotting limits the spread

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12
Q

what mechanical defences are involved in the skin?

A

tight junctions, longitudinal flow of air or fluid

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13
Q

what mechanical defences are involved in the gut?

A

tight junctions

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14
Q

what chemical defences are involved in the gut?

A

enzymes such as pepsin and low pH

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15
Q

what mechanical defences are in the lungs?

A

movement of mucus by cilia

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16
Q

what are the chemical defences of the lungs?

A

pulmonary surfactant, alpha defensins, cathelicidins

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17
Q

what mechanical defences are in the eye/nose/oral cavities?

A

tears and nasal cilia

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18
Q

what are the chemical defences of the eyes/nose/oral cavity?

A

enzymes in tears, histatins and beta defensins

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19
Q

what can a pattern recognition receptor exist as?

A

a cell surface PRR or soluble molecules

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20
Q

what is a molecular pattern?

A

low-molecular weight substances evoking the reactions of innate immunity with no memory

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21
Q

what are the different types of PAMPs?

A

pathogen associated, allergen associated, damage associated and tumour associated

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22
Q

what are some examples of pathogen associated molecular patterns?

A

bacterial flagellin, peptidoglycan, lipopolysaccharide, viral dsDNA

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23
Q

what are some examples of allergen associated molecular patterns?

A

allergens, IgE cross linking

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24
Q

what are some examples of damage associated molecular patterns?

A

damage, heat shock proteins, ATP, uric acid and heparin

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25
Q

what are some examples of tumour associated molecular patterns?

A

tumours, but may inhibit immunosurveillance

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26
Q

what are some examples of cell surface pattern recognition receptors?

A

scavenger receptors, lectin receptors, toll-like receptors

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27
Q

what do scavenger receptors do?

A

recognise cell debris

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28
Q

what do lectin receptors do?

A

recognise bacterial carbohydrates

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29
Q

what do toll-like receptors do?

A

recognise PAMPs and activate macrophages

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30
Q

what are some examples of soluble PRR’s?

A

pentaxins, ficolins and collectins

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31
Q

what category of a soluble PRR does C-reactive protein fit into?

A

a pentraxin

32
Q

what does C-reactive protein recognise as a molecular pattern?

A

pneumococci

33
Q

what molecules are not PRR’s but closely related?

A

complement C3b and C1q, Fc receptors

34
Q

what is the trigger for innate immunity?

A

patterns

35
Q

what cells are crucial for innate immunity?

A

phagocytes, NK cells, mast cells

36
Q

what is the definition of a pattern recognition receptor?

A

molecules expressed by cells of the innate system which are capable of sensing patterns and triggering reactions

37
Q

what are the 5 families of PRR’s?

A

toll-like receptors, C-type lectin receptors, NOD-like receptors, RIG-1-like receptors and AIM-2-like receptors

38
Q

what cells express toll-like receptors?

A

macrophages, neutrophils, dendritic cells, lymphocytes and epithelial cells

39
Q

what is the function of toll-like receptors?

A

after binding to ligands, most TLR’s transduce signals that eventually lead to the activation of inflammasome and pyroptosis

40
Q

what does TLR’s recognise?

A

PAMP’s and DAMP’s

41
Q

how does TLR’s provide a link between innate and adaptive immunity?

A

can also interact with antigens due to a pathogen bound to a TLR being engulfed and antigen presented

42
Q

where are CLR’s found?

A

bound to the cell membranes and mainly involved in fungal recognition and endocytosis

43
Q

what other PRR’s provide a link between two types of immunity?

A

CLR’s

44
Q

what are the main roles that CLR’s play in?

A

anti fungal, antimycobacterial and anti tumour immunity

45
Q

where are NOD-like receptors found?

A

in the cytosol

46
Q

where foes the term NOD come from?

A

nucleotide-binding oligomerisation domain

47
Q

what does NOD bind too?

A

nucleoside triphosphate

48
Q

what does NOD-1 receptors recognise?

A

peptidoglycan of gram negative bacteria

49
Q

what does NOD-2 receptors recognise?

A

intracellular muramyl dipeptide which is a peptidoglycan of G+ and G- bacteria

50
Q

what are NOD receptors responsible for?

A

takes part in inflammatory response, activates pro inflammatory cytokines, pyroptosis

51
Q

what role does NOD2 play in autoimmune diseases?

A

mutations in NOD2 can lead to chrohns disease or Blau syndrome due to overexpression

52
Q

where do RIG receptors exist?

A

in the cytoplasm

53
Q

what does a RIG receptor consist of?

A

RNA helices domains and capsize activation and recruitment domains (CARDs)

54
Q

what are the ligands for RLR’s?

A

viral PAMP’s and dsRNA

55
Q

what does activation of RLR’s lead to?

A

type I interferon production

56
Q

how does RLR activation work?

A

recognises the viral RNA and triggers cytokine production of the infected cell

57
Q

where are ALR’s located?

A

in cytoplasm and nucleus

58
Q

what are the ligands for ALR’s?

A

ds DNA of bacteria or viruses

59
Q

what does activation of ALRs cause?

A

formation of AIM2 inflammasomes and production of pro-inflammatory cytokines and type I interferons

60
Q

what is an inflammasome?

A

multiprotein intracellular complex that detects pathogenic microorganisms and activates pro-inflammatory cytokines

61
Q

what cytokines does inflammasomes activate?

A

IL1b and IL-18

62
Q

how do inflammasomes cause cell death?

A

cause pyroptosis

63
Q

what is NETosis?

A

neutrophil extracellular traps

64
Q

what are NET?

A

extracellular fibres of primarily DNA, produced by the outside of the cell that traps pathogens minimising damage to host cells

65
Q

what does NET release?

A

chromatin plus granule proteins outside of the cell

66
Q

how does the release of granule proteins increase efficacy of NET?

A

the net concentrates these proteins which destroys microbes and prevents diffusion into the host cell

67
Q

how is NET linked to lupus?

A

also cause the release of EC histone proteins

68
Q

what are the main roles of complement?

A

attraction of phagocytes, opsonisation, triggering mast cells, forming MAC complex and inflammation

69
Q

how does complement cause inflammation?

A

attraction of phagocytes via chemotaxis and triggers mast cells to release inflammatory mediators

70
Q

how does complement cause lysis?

A

forms MAC

71
Q

what is the main stage in enzyme pathway of complement?

A

cleavage of C3 into C3a and C3b

72
Q

what type of antibody activates complement?

A

IgM

73
Q

what activates classical complement pathway?

A

antibody and antigen

74
Q

what activates lectin complement pathway?

A

microbial carbohydrates

75
Q

what activates alternative complement pathway?

A

microbial components